immunology

Acquired adaptive Immunity

Immune protection can be: Natural=> when the body naturally encounters pathogens and mounts a response to their antigens. Artificial=>when the pathogen/antigen is introduced, or when the antibodies are directly supplied. Active=>if the body has an active roll in perpetuating the response. Passive=> if the body receives the antibodies/cells and the effect just lasts while the antibodies/cells are being supplied. Naturally Acquired Active Immunity: that which happens when the body naturally encounters a pathogen in the environment, mounts a specific response that can be enhanced by immune cellular memory. (either t or b memory cells or both) •Naturally Acquired Passive Immunity: Ig G that passes across the placenta during pregnancy remain in the blood stream of the newborn during the first days/months. Also, IgA is transferred to the baby via breast milk... no cellular memory •Artificially Acquired Active Immunity:vaccines present either just the antigens or attenuated pathogens to allow the body to mount a controlled and safe immune response against a specific pathogen. It produces cellular memory without disease. •Artificially Acquired Passive Immunity: when antibodies that have been prepared elsewhere (e.g. horse) are supplied to produce an immediate immune protection, for example when antiserais injected to protect against the toxic effect of snake venom....no memory

Antibody adaptive Immunity

Immunoglobulins (antibodies) B cell receptor can secrete the molecules to extracellular environment and then r called Immunoglobulins -they have Y shape where the base os constant and the tops/ ends of Y are variable sites that where ou WBC can genetic variations that have different specificities of the variable sites that can bind to different antigens ... so the variable sites that bind the antigens and the specific epitopes within the antigen are in the two tips of the Y and the two ends of the Y are identical •Recognize epitopes with great specificity. •Have two identical biding sites. •Five classes: Ig G (~80%; can cross the placenta and easily enter body tissues),Ig A (~10% in serum; transferred in secretions including breast milk), Ig M (~5%), Ig E (<0.5%), Ig D (<0.5%). -the same plasma cell can secrete Immunoglobulins of different classes with the same specificity •Function: Involved in the activation of the "Complement system" and inflammation process. Neutralization of toxins by binding to its active site. Stimulate phagocytosis by flagging specifically infected cells and/or bacteria (opsonization) Agglutination: using its two biding sites, antibodies can agglutinate pathogens or molecules to make them less active. Stimulate the action of NK cells by flagging infected cells for NK-mediated apoptosis, and/or cytotoxin release. Neutralization involves the binding of specific antibodies to antigens f (pic attached) third pic.. example of hemoglobin binding to the flagella of bacterium cell which has several levels of effect.. if it has flagella then it will no longer be able to move and transport itself and hemoglobins serve as flagging particles for further action of the WBC.... the variable part of the hemoglobin is bound to the area (green) and the constant regions are left exposed. this is great because once they recognize the constant region, they know to act against that

Antibody mediated adaptive Immunity

Involves the interaction with T-helper cells (Th cells) and a B cell (type of lymphocyte). B cells have cell receptors and can produce molecules called immunoglobulins (antibodies), they can use them as cell receptors (BCR = B cell receptor on the cell membrane) or secrete them to extracellular enviorment B cell has 2 regions.. one called the constant region (the same sequence of amino acids with the same coding in all hemoglobins) and the variable region at the tips of the Y shape that varies greatly due to genetic recombination A great variety of immunoglobulins can be produced. Each B-cell develops immunoglobulins with unique epitope specificity by ne antigen given by the variable region Effector cells are B-cells.

Elements of adaptive Immunity

Lymphatic system •System that carries Lymph to different sites of the body. It constitutes the "surveillance system" of the body. •Lymph: colorless, watery liquid that arises from fluid leaked out of blood vessels and occupies intercellular (interstitial) spaces. It is similar in composition to blood expect it has no erythrocytes. •The lymphatic system is composed of vessels and lymphatic tissue: lymphatic capillaries, thymus, bone marrow, lymph nodes, spleen, tonsils, adenoids. •Bone marrow: is rich in "stem cells" that can differentiate into erythrocytes, platelets and leukocytes. •Lymph nodes are rich in WBC including B and T lymphocytes. •Is where a number of cellular process related to maturation, selection and activation of adaptive immune cells happen. Antigens •The adaptive immune system recognizes "antigens", not full microorganisms. •Antigens: molecules that the immune system recognizes as foreign or not, and that determine if an immune response is induced. •An antigen that elicits an immune response is called an "immunogen". •Specifically the adaptive immune system recognizes a small portion of the antigen molecule called "epitope" or "antigenic determinant". Mayor Histocompatibility Complex (MHC)How does the body know if something is foreign or part of itself ? •The Mayor Histocompatibility Complex (MHC) is set of host-cell surface proteins .•MHC proteins are antigens found on the cytoplasmic membrane of the cells of most vertebrates. •Two types: MHC class I and MHC class II. •MHC class I: are present in all human cells except red blood cells (erythrocytes). (one anchor across the cell membrane of the host cell) •MHC class II: are present in "antigen presenting cells" (APCs) such as B-cells, dendritic cells andmacrophages.. (two anchor across the cell membrane of the host cell) antigen binding cleft: space where they can attach present an antigen and this is key in the way white blood cells can proceed (both class one and class two have this and can present antigens) MHC I are found on all nucleated body cells, and MHC II are found on macrophages, dendritic cells, and B cells (along with MHC I). The antigen-binding cleft of MHC I is formed by domains α1 and α2. The antigen-binding cleft of MHC II is formed by domains α1 and β1.. pic attached

PAMPs, PRRs and TLRs

Phagocytic cells can recognize opsonized pathogens and/or pathogen-associated molecular patterns (PAMPs) => highly conserved molecules that are common to many different pathogenic microbial cells (but are absent in host cells). •PAMPs examples: LPS , peptidoglycans, flagellin, viral nucleic acids and lipopeptide (common bacterial membrane protein). •Phagocytic cells express pattern recognition receptors (PRRs) capable of recognizing various PAMPs. These PRRs can be found on the plasma membrane or in internal phagosomes. •Some PRRs are toll-like receptors (TLRs) =>recognize PAMPs and communicate with the phagocyte's nucleus to elicit a response. •When a PRR recognizes aPAMP,it sends a signal to the nucleus that activates genes involved in: phagocytosis cellular proliferation production and secretion of antiviral interferons and proinflammatory cytokines enhanced intracellular killing

Superantigens

Superantigen (SAg): an exotoxin that trigger an excessive, non-specific immune response. Non-specific stimulation of T-cells => massive cytokine release and can cause toxic shock syndrome T-cell mediated response has evolved to be specific (adaptive immunity), lack of specificity produces a systemic response that can be life-threatening. Cytokines magnify the immune response and recruit macrophages. A number of proinflammatory cytokines are produced like interferon gamma (INT-g) andtumor necrosis factor alpha (TNF-a) . Produces shock syndrome: high fever, low blood pressure and eventually multiple organ failure. Examples: toxic shock syndrome protein by Staphylococcus aureus; mitogenic and pyrogenic toxins by Streptococcus pyogenes. a) The macrophage in this figure is presenting a foreign epitope that does not match the TCR of the T cell. Because the T cell does not recognize the epitope, it is not activated... what should normally happen is your have the macrophage or dendritic cell and then it encounters a pathogen and processes it rhgouh phagocytosis and then with the remains of the pathogen, it encounters an antigen and processes the antigen and mounts it in an major class 2 molecule and then the antigen exposes a specific epitope that can be recognized by a T cell receptor of a T cell and then we have recognition and that T cell can be activated to differentiate into a t helper 1 or t helper 2 type cell (b) The macrophage in this figure is presenting a super-antigen that is not recognized by the TCR of the T cell, yet the superantigen still is able to bridge and bind the MHC II and TCR molecules. This nonspecific, uncontrolled activation of the T cell results in an excessive release of cytokines that activate other T cells and cause excessive inflammation... super antigens force the interaction between the major class 2 molecule and the T cell receptor without any specific epitope or any antigen mounted at all ... so the recptor still produces cytokines to kill cells but it gets unspecifically stimulated so it created inflammation and kills cells in a nonspecific fashion and against cells that are not infected which leads to severe clinical situations that can be fatal

Cell mediated adaptive Immunity

T-cell (type of lymphocyte) can differentiate into: cytotoxic T cell (Tc or CTL), T helper cells (Th), memory T cells and regulatory T cells. Each T cell develops TCR (T cell receptors) with unique epitope specificity. Cell mediated process: 1.Th0 interacts with the APC, if the Th is induced to differentiate into aTh1a cell mediated adaptive response is elicited. Th1 cells become CTL 2.Cytotoxic T-cells (CTL) are induced to take the cytotoxic pathway against any cell presenting that specific epitope on their surface (on a MHC I molecule). 3.CTL release "cytotoxins" can induce Apoptosis of target cell and/or they can directly kill infected cells by the production of perforins. 4.After the infection has been controlled, some of the CTL cells become "memory T cells", which can persist for long periods of time in lymphatic tissue. 5.Memory cells require less stimulation to mount a specific response against that specific epitope at a later encounter. 6.Effector cells are T-cells.

phagocytosis

The stages of phagocytosis include the engulfment of a pathogen, the formation of a phagosome, the digestion of the pathogenic particle in the phagolysosome, and the expulsion of undigested materials from the cell. -phagocytic cells (macrophages and endrtic cells (the professional phagocytic cells of the body)..once a phogocyte recognizes a cell as something it needs to get rid of, it educes phagocytosis ( it uptakes a particle with the intent of killing it ) firs thing that happens is thatt the cell membrane evaginates the membrane of the cell wall and creates a phagosome (body) and then in the cytoplasm of the phagocytic cell, a lysosome is recruited (an organelle of phagocytic cells that contains other digestive enzymes that can break down proteins, nucleic acids, etc... most of the content is broken down by lysosome)) lysosome fuses with phagosome and creates phagolysosome where the bacteria come in direct contact with all the enzymes in the lysosome and remain in contact for a period of time where all the components of bacteria cell are broken down. and when the infectious particles become no longer infectious, the debris are secreted to the extracellular environment of the phagosome and often times the release pathogenic particles activates other immune process such as recruiting more white blood cells to that site

Immunity

White Blood Cells (WBC)Leukocytes => most can exit blood capillaries and move to infection sites (diapedesis). •Basophils: involved in inflammatory by degranulation (e.g. histamine) => acute and chronic allergic reactions. •Neutrophils: phagocytosis and degranulation (e.g. antimicrobial molecules). •Eosinophils: control parasitic infections, involved in allergy and asthma, have degranulating and phagocytic properties. -granulocytes (Basophils, Neutrophils, Eosinophils) can degranulate.. the granules can carry types of inflammation mediators, histamine, antimicrobial molecules and all of the contents of the genaulocytets are deigned to recruit white blood cells to the site of infection and to inactivate the pathogens •Monocytes: can differentiate into macrophages or dendritic cells (both are professional phagocytes). Immunity orangesdms.wikispaces.com •Lymphocytes: Natural Killer cells (NK): innate immunity, respond to viral infected cells, they induce Apoptosis (controlled cell death where contents remain contained). ( a cell that interacts with a NK starts a process of controlled death.. usually Nk will induce apoptosis on a cell of the body that is infected with a pathogen and this renders the cell dying and forms little packets of cell that is rounded by cell membrane so the intracellular contents are contained) T-cells: cell mediated adaptive immunity ... role in cell mediated and antibody mediated immunity B-cells: humoral (antibody-mediated) adaptive immunity.

drawing of macrophage

antibodies serve as opsonins and inhibit infection by tagging pathogens for destruction by macrophages, dendritic cells, and neutrophils. These phagocytic cells use Fc receptors to bind to IgG-opsonized pathogens and initiate the first step of attachment before phagocytosis the receptors that macrophage has to recognize the constant part of hemoglobin on their membrane... there is an extracelluyla end and intracellular end and once the extracellular end is bound to the binding molecule, it will trigger a response within the cell which produces a change in behavior. the part that has the antigen eiptiope biding cleft is going too recognize the pathogen and bind to it, but the constant region of the hemoglobin is going to stay the same and macrophages have receptors )N) that recognize the constant region of the Immunoglobulins that are exposed to the extracellular environment of the pathogen and the message is :this is something I need to take out and destroy. so, the macrophages are stimulated to innate phagocytosis which will render the inactivation of the pathogen

Innate Immunity

complement system: >30 proteins that circulate in blood (plasma) Two modes of action: 1.Complement proteins can coat pathogens (opsonization) => stimulate phagocytosis. 2.Complement cascade can create multiple pores in phospholipid bilayers in pathogen cell => cell lysis. Trigger inflammation and fever. Inflammation •Non-specific response to tissue damage (heat, chemicals, abrasions, cuts, pathogens, etc.) •Symptoms (and signs): swelling, redness, heat and pain. •Initiated by WBC production of cytokines •Amplified by inflammation mediators such as histamine (basophils and mast cells) and prostaglandin (by many different cells). •Vasodilation and increased permeability of blood vessels •Diapedesis: passage of blood cells through the intact walls of the capillaries. •Increased production of protective chemicals (such as antimicrobial peptides) •Increased migration of phagocytes (resolve or contain infection) ****once the bacterial infection has been contained by WBC and phagocytic cells recruited to the site of infection, the second step is to have mechanisms of tissue repair... •Mechanisms of tissue repair inflammation is in 2 forms... Acute inflammation (evolves and resolves fast) is usually beneficiary. Chronic inflammation usually causes tissue damage and chronic disease. Fever •Body temperature above normal (>37 degrees Celsius = 98.6 degrees Fahrenheit) •Pyrogens are chemicals that induce fever by stimulating the hypothalamus to increase the body temperature. •Pyrogens Exogenous: made by bacteria or viruses and processed by WBC .Endogenous: some cytokines like interleukins (IL-2 and IL-6), INF-gand Tumor necrosis factor alpha TNF-a •It is thought that higher temperatures enhance the effect of interferons, inhibit the growth of some microorganisms, improve the performance of phagocytes and lymphocytes. •Fever that is too high can denature body proteins and inhibit nerve impulses (hallucination, coma, etc.) -some believe that fever is brought about in order to enhance and advance the activity of white blood cells -heat to a range, is a catalyst and can improve the biochemical reactions in general -if a fever is too high, some proteins can get denatured.. and that is correlated to irreversible damages of some nerves of the body and so high fevers can produce anythewre between hallucination/ coma

Antibody mediated pathway

naive cell: in organge t cell receptor: baby blue dendritic cell: purple mayo class 2 molecule: grey antigen: red triangle we start with the antigen (specific one in this drawing by red triangle and whole pathogen is represented by green circle with spikes) the pathogen is recognized by a professional antigen presenting cell (like macrophage) and it is phagocytosed and I not able to invade phagocytosis and when it is completely killed, a few antigen molecules that are in the remaines of the pathogen after the phagolyososome has comepltley inactivated the pathogen, goes on to the antigen processing that ends with the mounting of the antigen on a mayor class 2 molecule our professional antigen presenting cell presents the antigen mounted on a mayor class 2 molecule to a naive t helper cell there are co-receptor interactions and depending on how the interaction goes, our t helper cell develops and differentiate into a T cell helper 2 cell instead of 1 (main difference between 1 and 2 is the type of interaction they have with the professional antigen presenting cell and the type of cytokines they are induced to secrete bc they will have different affects on WBC).. after it becomes a T cell helper 2 it migrates to different tissue and looks for a B cell that has already encounbtered that same type of antigen and processed it and is presenting it in a mayor class 2 molecule so our t helper cell upon the 2nd interactionwieh the same antigen mounted on a mayor class 2 molecule and the message received is that this is an antigen we need to act against and the T cell is having a second confirmation that this is the right antigen to act upon and produces a series of cytokines that are going to induce our B cell to differentiate into a plasma cell and the B cell turns into a machine of secreting antibodies/ hemoglobins like crazy and they keep dividing and producing more plasma cells and as moe come about, they become more specific and efficient in finding and binding that antigen.. so, this huge production of hemoglobins helps to inactivate the infection but once the infection has been resolved, the plasma cell diferneitates into a memory B cell and lives in a dormant mode in the lymphatic tissue (this waits to encounter that same antigen at a later time and because the memory B cell has already gone through this process, in the future it will be able to amount a much rapid and efficient response against that specific antigen) THIS IS CALLED IMMUNE MEMORY.. memory of antsy mediated pathway (it Taylors specific responses that the body can keep memory of and that memory happens form of t memory cells for cell mediated pathway and B memory cells for antibody mediated pathway )

The initial interaction of the APC and a naïve T cell determine the pathway

2 pathways adaptive immunity can be activated.. cell mediated and antibody mediated first starts when an antigen first interacts with an antigen mediated cell the apc is in the purple in the middle... this processes the pathogen by phagocytosis and ends up mounting the antigen (the red triangle) in presents it on its surface then the apc interacts with the T cell (a T cell that hasn't decided weather to go through the cell mediated pathways or antibody mediated) and the nature of the interaction determined which pathway and often has to do with the nature of the antigen (and what kind of signal the T cell is going to recieve... the t helper cell may differentiate into a t helper 1 or 2 and what differs between the two is what kind of cytokines they secrete.... usually after an interaction with a virus we can a T cell helper 1 that secretes different cytokines and other types of pathogens like bacteria secrete different cytokines) the effector cells in the cell mediated pathway (on left side of pic) are T cells and the effector cells of the antibody mediated pathway (on right side) are B cells B cells and T cells both originate in bone marrow, but B cells also mature and require the receptors in the bone marrow.. whereas T cells leave the bone marrow and travel to the thymus where they develop there cell receptors and mature ... then both go and migrate to lymphnodes where they interact with antigen presenting cells and go through processes of selection and specificity lymphocytes when they are maturing and producing there receptors, eukaryotes have the ability of recombining their genes in a way where we can generate a great variety of different types of receptors (specifically lymphocytes are capable of recombining the genes that code for the proteins that make up their cell receptors in a way where they can generate an endless amount of cell receptors with different specificities).. it is important that only lymphocytes that recognize themselves as self and not amounting an immune response against self will be allowed to continue and clone and multiply and those will eliminated to prevent the body from generating an autoimmune disease

Adaptive Immunity

Adaptive immunity (specific). Third line of defense (cell mediated and antibody mediated) •Ability of the host to recognize and defend against specific invader •Specificity: process tailored to pathogen •Inducibility: activated by that specific pathogen •Clonability: once pathogen is recognized, cells of the adaptive system form many identical (clone) cells that are equally adapted to that pathogen. •Memory: immunological memory is the ability to respond faster and more effectively to subsequent encounters with the same pathogen.

how opsonized my Immunoglobulins is able to enhance the killer affect of natural killer cells

Antibody-dependent cell-mediated cytotoxicity (ADCC) : antibodies bind to a large pathogenic cell that is too big for phagocytosis and then bind to Fc receptors on the membrane of a natural killer cell. This interaction brings the NK cell into close proximity with the help pf Immunoglobulins, where it can kill the pathogen through release of lethal extracellular cytotoxins.

Elements of adaptive Immunity pt 2

Antigen presenting cells (APCs) •Macrophages, dendritic cells and B-cells are "professional APCs". •After phagocytosis/internalization, APCs undergo an "antigen processing" phase => foreign epitope is presented at the APC membrane on a MHC II molecule. •APCs with epitopes presented on their cell membranes, migrate to the lymphatic system and interact with cells of the adaptive immunity .•This interaction induces cells' maturation, selection and induction. •Other body cells can present antigens "non-professionally" on MHC I molecules Self epitope on MHC I = no response Pathogen epitope on MHC I = immune response. when a WBC interacts with a cell that is presenting an antigen on a major class 2 molecule, the message received is " I am warning you that this is a feature u should be looking out for and when you recognize it, you should destroy it" a WBC that interacts with the cell that has a foreign pathogenic antigen mounted on a foreign class one molecule, the message received is "help me, I am contaminated, this is a pathogen I am infected with" and then usually apoptosis occurs

Cytokines and immunity

Cytokines: usually a small protein secreted by one cell that alters the behavior or properties of another cell (and/or of the secreting cell itself). •Have roles both in innate and adaptive immunity. •Often induce production of inflammatory mediators such as histamine and prostaglandins. •Examples: Interferon gamma (IFN-g): can block viral replication, activates macrophages, activates antigen presentation in antigen presenting cells, promotes NK cell activity. Interleukins4 (IL-4): activates B-cells Interleukins12 (IL-12): activates T-cell of the cell mediated adaptive response, also enhances cytotoxic function of NK cells. Tumor necrosis factor alpha (TNF-a): part of the "acute phase reaction proteins" (associated with inflammation) in plasma, is produced by activated macrophages (and other cells). Can induce fever, apoptosis and inflammation. cytokines protect neighbor cells from suspected infections by viral particles.... as seen in pic

Degranulation and Apoptosis

Degranulation= property of granulocytes.. where the granulocytes are able to exit the blood stream by the apedasis... it is recruited by chemical signaling that call the granulocyte to the site of infection and when it reaches the site of infection, the granulocyte is able to degranulate and release the content of the granules (anything from inflammatory mediators to antibacterial peptides) apedasis is important in immunity apoptosis is induced by cell receptors of the NK and the recipient cell and the host cell that is affected and receives the signal to do apoptosis and starts the process by which is degregates all the major components of cells wo where all the contents of the cell are no longer viable ... the infectious particle gets contained in its own little pocket to try and operate from the other important genetic material

Innate Immunity

For a pathogen to cause disease it most: 1.Gain access to the body 2.Attach itself to host cells so it won't be shed 3.Remain undetected by the host's defense system long enough to cause harm. (penetrate and affect) Skin composed of two layers: epidermis and dermis. (first barrier the microorganism will find when trying to enter our body... skin and mucosa) -biggest differences between epidermis and dermis is that the epidermis is made up of dead cells and dermis is made up of live cells Epidermis Composed of multiple layers of tightly packed dead cells (with Keratin) that constitute a physical barrier for most pathogens. Continual renewal, discards microorganisms attached to flaking dead skin. Contains phagocytic cells called "dendritic cells", this cells can engulf (phagocyte) and deactivate pathogens. Dermis (2nd layer in our skin) Cells of the dermis are rich in collagen. Collagen is a protein that forms fibers. Collagen fibers give skin strength and pliability (prevent jabs and scrapes). Antimicrobial peptides (AMPs): dermal cells and sweat glands secrete small peptides (~20 a.a.) (e.g. "defensins") (broad spectrum: G+ve & G-ve bacteria, fungi, virus). Lysozyme: enzyme present in human secretions like tears, saliva, human milk, sweat, mucus, etc. Enzyme that hydrolyzes sugar-linkage in peptidoglycans (G+ve bacteria are most susceptible). (effective even if the cell is not dividing) Sebaceous/oil glands: secrete "sebum" (fatty acids) that keeps skin pliable and pH low (~pH=5) that is harmful to pathogens -these oils/ liquids sit in dermis but they end up reaching the epidermis and lubricate the epidermis Mucous Membrane (Mucosa) •Covers all the body cavities that are open to the environment (respiratory, urinary, reproductive and digestive tracts, as well as ears and eyes). -gives an extra layer to all these lives cells and keeps it moist •Secrete mucus (glycoproteins, water, electrolytes),which can cover and inactivate microorganisms •Epithelium (surface layer of mucosa) is composed of live cells that are more susceptible to infections than those of the epidermis. •Ciliated epithelial cells can physically displace microorganisms form the body (e.g. respiratory tract). •Mucosa can also secrete antimicrobial peptides. Microbiota (human flora) •Normal human flora protect our body from pathogens by "microbial antagonism". •Microbial antagonism: the growth of one microorganism prevents the growth of another (for example by keeping the pH too low for most pathogens to grow).

Defense in blood

•Blood: liquid tissue composed of cells and plasma •Plasma: water, electrolytes, clotting factors, acute-phase proteins, complement protein and cytokines. •Serum: plasma without clotting factors... what is left in blood when we take away from plasma the clotting factors •Blood cells (originate in the bone marrow) Erythrocytes: or red blood cells (RBC) containing hemoglobin (which carries oxygen to body tissues). Platelets: not full cells but portions cells, are involved in clotting. Leukocytes: white blood cells (WBC), directedly involved in immune defense (innate and adaptive). Five main types: Basophils, Neutrophils, Eosinophils, Monocytes, Lymphocytes.

Immunology

•Immunology: a branch of biology that studies the host defense mechanisms against disease. It involves a variety of structures and processes. •In general, there are 3 lines of defense and 2 types of immunity •Innate immunity.. we are born with (non-specific) -First line of defense: skin, mucous membrane (mucosa), normal microbiota. -Second line of defense: specialized cells (like phagocytes), antimicrobial molecules (like interferons), and processes (like inflammation and fever). •Adaptive immunity... we acquire after we have seen infectious agents (specific). Third line of defense -Ability of the host to recognize and defend against non-self. -Its is a characterized by specificity of the response and immune "memory" .-Main actors are B-lymphocytes (antibody immune response) and T-lymphocytes (cellular immune response). -ability of the cells to recognize cells of the body from not cells