Chapter 19 Part 3

Response of reduction of NK cells

Immunological surveillance is compromised -Cancer has a higher risk

IgA

In glandular secretions such as mucus, tears, saliva, and semen

T cell activation by infected cells

Inactive T cells have receptors that recognize either Class I or Class II MHC proteins when bound to specific antigen It will only detect it if the MHC protein contains the antigen that that T cell is programmed to detect --This is called antigen recognition

Allergies

Inappropriate (or excessive) immune responses to antigens (allergens) Sensitization and activation of B cells to allergens leads to a production of large quantities of IgE

Gaft rejection

Recipient Cytotoxic T cells become activated and attack MHC proteins of donated material Reduction in immune response sensitivity (immunosuppression) by drugs can increase transplant success Ex: Cyclosporin A inhibits helper T cells

Primary response of antibodies

Response to initial antigen exposure: delayed due to time to activate specific B cells Antibody titer (level of antibody activity) peaks 1-2 weeks after initial response

Examples of autoimmune disorders

Rheumatoid arthritis (attack on connective tissue around joints) Insulin-dependent (type I) diabetes mellitus (attack on pancreas) Multiple sclerosis (attack of myelin)

Antibodies

Small soluble proteins that bind to specific antigens; they may inactivate the antigen or trigger another defensive process

Full activation of B cells occurs

When activated helper T binds to sensitized B cell antigen-Class II MHC complex

Specific and non-specific defenses:

Work together to defeat pathogens

T cell activation and cell division

Three CD8 cells produced 1. Cytotoxic T cells (most) 2. Memory T cells 3. Suppressor T cells

Memory T cell

Upon 2nd exposure to antigen, become cytotoxic T cells

IgG

(80% of all antibodies) against many viruses, bacteria, and bacterial toxins

Steps of CD8 recognition

1. Antigen recognition 2. Costimulation 3. T cell activition and cell division

Result of allergies

1. Localized inflammation, pain, itching -Ex: hypersensitivity reaction of allergic rhinitis --Ex: hay fever and other pollens 2. Systemic (allergen in blood stream, symptoms are widespread -Ex: anaphylaxes (circulating allergens causing widespread vasodilation through mast cell activation

Class II MHC protein activation

1. Phagocytic APCs engulf the extracellular pathogens 2. Lysosomal action produces antigenic fragments 3. ER produces Class II MHC proteins 4. Antigenic fragments are bound to class II MHC proteins 5. Antigenic fragments are displayed by class II MHC proteins on the plasma membrane

Immunodeficiency diseases result form

1. Problems with lymphoid organ and tissue development 2. An infection with a virus that depresses immune function -example: acquired immune deficiency syndrome caused by human immunodeficiency virus (HIV) that infects CD4 cells 3. Treatment or exposure to immunosuppressive agents like radiation or drugs

Autoimmune disorders

Activated B cells B cells make antibodies against "self-" antigens on body cell tissues=autoantibodies -likely to arise from body cell antigens being too similar to specific foreign antigens

Activation of complement

After antigen binding, complement also can bind to the antibody accelerating the complement cascade

IgM

Anti-A and Anti-B are examples

Neutralization

Antibodies bind viruses and bacterial toxins Prevents them from affecting body cells

Overview of MHC activation

Antigen presentation by Class I MHC proteins is triggered by viral or bacterial infection of body cell Infection leads to abnormal peptides Abnormal peptides are incorporated into Class I proteins as they are synthesized in the ER After export to the golgi, MHC proteins reach plasma's membrane within transport vesicles The abnormal peptides are displayed by class I MHC proteins on plasma membrane

IgE

Attach to basophils and mast cells causing release of histamines

Attraction of phagocytes attached to antibodies

Attract eosinophils, neutrophils, and macrophages

Stimulation of inflammation

Basophil and mast cells stimulation to release histamine

Cytotoxic T Cells

Destroys infected and abnormal cells Target cells must have specific Class MHC proteins -Release of perforins and activation of target cells self-destruction genes for death (apoptosis)

Classes of antibodies

Differences in constant segments 1. IgG 2. IgE 3. IgD 4. IgM 5. IgA *all formed in human milk, but IgA is most abundant

Response of T cells becoming less responsive with age

Fewer cytotoxic T cells

Constant segment of Antibodies

Form the base

Secondary response of antibodies

From memory B cells to specific antigen Antibody titers increase more rapidly (and each higher concentration especially IgGs)

Major histocompatibility complex (MHC) proteins

Genetically determined membrane glycoproteins present on all cells Foreign antigens attach to these MHC proteins and appear on cell surface T cells bind antigens MHC complex and become activated

Class II MHC proteins

Only in membranes of antigen-presenting cell (APC) ex: macrophages Create complex with phagocytized pathogens

Triggering an immune response

Involves Major Histocompatibility Complex (MHC) proteins

Suppressor T cell

Limit response of other T cells and B cells

Agglutination

Linking of multiple pathogens by antibodies creating an immune complex

B cell activation

Must bind a specific antigen Antigens brought into the cell through endocytosis/phagocytosis, and then placed on the surface of a cell bound to Class II MHC proteins This process is sensitization or the preparation to undergo B cell activation

Primary antibody actions

Neutralization Activation of complement Stimulation of inflammation Agglutination Attraction of phagocytes

CD4 markers

On CD4 T cells Respond to class II MHC proteins

CD8 markers

On CD8 T cells Respond to class I MHC proteins

Costimulation

Physical or chemical stimulation of T cell in addition to the Class I MHC molecule

Activated B cells produce

Plasma cells (activated B cells: produce antibodies) Memory B cells (inactive until 2nd exposure to antigen)

IgD

Plays a role in B cell sensitization

Variable segment of antibodies

Possess antigen binding sites Differences in amino acid sequences produce variability needed for different antibodies Ex: binding a bacterium

Cause of less T cells with age

Possibly due to thymus atrophe

Class I MHC proteins

Present on all cells and create a complex when cell is infected with bacteria or viruses

Age-related reductions in immune activity

T cells become less responsive B cells respond less due to less helper T cells (vaccinations highly recommended for elderly individuals) NK cells reduced

CD (Cluster Differentiation) markers

The membrane proteins involved in antigen recognition CD8 markers CD4 markers