Chapter 8
_____ cells remain in, rather than leave, the secondary lymphoid organs in which they differentiated
CD4 Tfh
IL-4 is induced in a CD4 TH2 cell under the direction of the transcription factor
GATA-3
Binding of ______ to ___________ induces T cell proliferation and differentiation of activated T cell
IL-2; the high affinity IL-2 receptor
naïve lymphocytes homing to lymphoid tissue use _________ to bind to CD34 and GlyCAM-1 on high endothelial venules
L-selectin
which of the following characteristics permits activated CD8 T cells to destroy any cell type harboring viable and replicating pathogens such as viruses?
MHC class I molecules are expressed ubiquitously by most nucleated cells
describe the maturation of dendritic cells (DCs) and changes in their capacity for PAMP recognition, protein expression (B7-1/2), antigen take-in, MHC, migration, antigen presentation?
Maturation of dendritic cells is associated with changes in their form and function. During maturation dendrites become high elaborated facilitating interaction with T cells in the cortex of the lymph node. Signals induced by interactions of CCL21 with CCR7 will cause pathogen-loaded and migrate the dendritic cells to leave the lymph. These signals will also induce maturation of dendritic cells. During maturation expression of MHC class I and II molecules increases this will lead to an abundance of stable, long lived peptide:MHC complexes on the surface. Mature dendritic cells provides nursery for propagation and maturation of effector T cells
expression of IFN-γ is induced in a CD4 TH1 cell under the direction of the transcription factor.
T-bet
if a non-professional antigen-presenting cell that lacks co-stimulatory molecules presents peptide: MHC complexes to a T cell specific for that peptide then:
T-cell tolerance occurs as a result of anergy
what helper T cell subset is MOST likely to be preferentially generated in response to a virus infection?
TH1
Identify the MISMATCHED pair
TH1: GATA3
all of the following statements regarding interleukin-2 (IL-2) or its receptor are true EXCEPT:
the low-affinity IL-2 receptor is a membrane-bound heterodimer composed of α and β chains
Which of the following statements regarding leprosy is FALSE?
the patient makes a TH2 response that clears the mycobacteria from the body
select the correct statement concerning TH17 cells in the figure
the transcription factor RORγT turns on expression of the IL-17 gene
all of these statements refer to regulatory T cells EXCEPT
they enhance the production of a new effector T cells
which of the following describes an activated dendritic cell upon arriving in a lymph node
bears highly elaborated finger-like processes called dendrites
dendritic cells take up, process or present antigen by each of the following routes except
cross-presentation from the MHC class I pathway to the MHC class II pathway
which of the following contributes to the activation of naïve CD8 T cells?
dendritic cells
follicular helper T cells are a recent discovery in the helper T-call lineage. What is the primary role of TFH cells?
to help B-cell development in germinal centers
The area of contact between membranes of a T cell and an antigen-presenting cell where a clustering of protein-protein interactions occur is called a(n)
immunological synapse
Parents who were distantly related to each other brought their 11-week-old infant, Kristen, to the emergency room after she had a seizure accompanied by a persistently high fever and running nose. Her liver and spleen were enlarged. Laboratory tests revealed abnormally high levels of lymphocytes and of the cytokines IFNγ, TNF-α, and IL-6. The physician suspected a primary or congenital immunodeficiency. A frameshift mutation in the perforin gene PRF1 was found on both chromosomes. Kristen was diagnosed with the rare, potentially life-threatening disease known as familial hemophagocytic lymph histiocytosis (FHL). Kristen was given immunosuppressive therapy followed by a matched unrelated hematopoietic stem cell transplant. Two years later Kristen is a healthy toddler. Which of the following would NOT be likely features of FHL?
impaired cytotoxic activity of CD8 T cells.
all nucleated cells express MHC I and present viral antigens (if the cells are infected by viruses) but infected DCs rather than other infected cells can activate naïve CD8 T cells. Why?
infected DCs can activate naïve CD8 T cells because infected DCs with some type of virus can activate a naïve virus-specific T cell on their own. The DC will send a strong signal to activate the CD8 T cell to effector status. Activated virus-specific CD8 T cells makes IL-2 creating its own proliferation and differentiation
PDL-1 can initiate a negative costimulatory signal to T cell by binding PD-1 on the T cell surface. Cancer cells evade T cell killing by expressing PDL-1. What advantage would the expression of PDL-1 have in a tumor cell avoiding the immune response?
tumor cells can avoid being killed by activated cytotoxic T cells
what are the three signals for T cell activation? What are their roles
* Signal 1= clusters T-cell receptor and a co-receptor to initiate signaling within a T cell. It will activate macrophages. * Signal 2= intracellular signaling pathways initiated by the T-cell receptor complex, CD4 co-receptor, and CD29 co-stimulatory receptor. Killing of infected "target cells". * Signal 3= cytokines. Depending on which cytokines are present when the T cell is activated different outcomes can occur such as cytokines sending the T cell down a different development pathway or activate a cytokine response system.
what is T cell homing? Describe events occurred in T cell homing.
* T cell homing is a process in which naïve T cells leave the bloodstream and enter T cell zone of lymph nodes. * Events in T cell homing includes naïve T cells entering a high endothelial venule then L-selection binding to GlyCAM and CD34 attaching to the T cell to the endothelium. Next, the LFA-1 will be activated by chemokine and bind to ICAM-1. The lymphocyte will then leave the blood and finally enter the lymph node
describe those distinct helper T cells and how they are developed from native CD4 T cells and effector function (fate-specific cytokines and signature transcription factor). Explain their possible cross regulation in differentiation.
* Th1= T-bet is defining transcription factor. IL-12 and IFN-γ are the cytokines that induce differentiation * Th2= GATA3 is defining transcription factor. IL-4 is the cytokines that induce differentiation * Th17= RORγT is defining transcription factor. IL-6, TGF-β, IL-23 are the cytokines that induce differentiation * TFH= Bcl-6 is defining transcription factor. IL-6, IL-21 are the cytokines that induce differentiation. * Treg= FoxP3 is defining transcription factor. TGF-β is the cytokines that induces differentiation
how will activated CD8 T cells kill infected target cells? Virus-infected cells attack and killed by effector cytotoxic T cells are often surrounded by healthy tissues, which is spared from destruction. Explain the mechanism that ensures that cytotoxin T cells kill only the virus-infected cells (the target cells)
* activated CD8 T cells kill infected target cells in 4 steps. In the first step is the recognition of antigen in which naïve CD8 T cell is activated. The second step is proliferation and the third step is differentiation. Proliferation and differentiation of activated CD8 T cells. The final step is effector function. The effector CD8 T cells recognize and kill virus infected epithelial target cells. * cytotoxic T cells kill their target cells by inducing apoptosis. The cell commits suicide within. As a result, the cell shrivels and shrinks while keeping its contents inside. Five granzymes cleavage reactions that leads the activation of nucleases within the target cell.
give a checkpoint blockade cancer therapy and explain how it works (do some search)
* checkpoint inhibitor for cancer therapy is mAb, PF-1, PK-L1/2, CTLA-4. * works to help the body immune system to recognize and attack cancerous cells
you have just been infected with an intracellular bacterial pathogen (such as Listeria monocytogenes). In mounting an immune response against the pathogen, which subset of CD4+ T cells will be produced preferentially? What polarizing cytokine will favor the production of this subset? What effector will be produced by this subset?
* subsets that will be produce are TH1, TH2, TH17, TFH, and Treg. * polarizing cytokines that will be favored in the production of the TH1 subset are IL12. * effector that will be produced by this subset is IL2 and IFNγ.
talk something about adjuvants, good and bad (Co-stimulatory Signaling vs. immune responses. You can do some searches)
* trigger the innate immune response and establish a state of inflammation at the site of vaccination. Inflammation is necessary for initiating an adaptive immune response against the antigens in the vaccine. * induce co-stimulatory activity in the dendritic cells which occurs during the innate immune response to infection. Will actively prevent generation of an adaptive immune response
the co-stimulatory molecule ____ on professional antigen-presenting cells binds ______ on the surface of naïve T cells
B7; CD28