Block 2 Immunology Sloma W Explanations

An epitope is the Part of the antigen recognized by antibody OR a Peptide recognized by the T cell receptor

This question is simply asking about how T cells recognize antigen and what type of antigens they can recognize.
T cells = pep-T-ides

E : Antibody binding to antigen can trigger all of the events described in A‐D. Recall that T cells are
activated when they encounter their specific antigen presented in MHC class I or II by antigenpresenting
cells. While the B cell may become activated when surface‐bound antibody binds its specific
antigen and then go on to present the antigen to the T cell, the activation of the T cell is a consequence
of presentation of the antigen by the B cell, not a direct consequence antigen binding to antigen.

Immunoglobulin G (IgG) is the most abundant immunoglobulin isotype in the serum. It
can cross the placental barrier but does not bind to the B-cell plasma membrane. It exists as a
monomer, functions to activate complement, and acts as an opsonin

Adjuvants are Thought to: Prolong the persistence of the antigen AND Stimulate or modulate immune cells AND Enhance macrophage function

Without surface‐bound antibody expression, a B cell cannot become activated. Surface‐bound
antibody molecules serve as the antigen‐recognition receptor for B cells.

Interferon -y activates macrophages, as well as natural killer (NK) cells and T cytotoxic cells, enhancing their phagocytic or cytotoxic activity or both.

cytotoxic cells are CD8+. CD28 molecules are present on TH 1 cells. Interferon (IFN)--y is
released by TH1 cells, and they also assist macrophages in killing microorganisms.

This question relies on the recognition that MHC class II molecules present exogenously‐derived antigens.
In all answer choices except D the cell is infecting a cell that does not express MHC class II.

T lymphocytes are preferentially located in the paracortex of lymph nodes, whereas B lymphocytes
are found in lymphoid nodules located in lymph nodes, tonsils, and the spleen.

Individuals allergic to penicillin produce immunoglobulin E (IgE) antibodies.
The cells that manufacture IgE are plasma.
After an antigenic challenge, proliferation and differentiation of B cells give rise to plasma cells and B memory cells.

T helper cells produce a number of cytokines that affect other cells involved in both the
cell-mediated and the humoral immune responses.
T helper cells possess antigen-specific T-cell receptors (not antibodies) on their membranes. These cells recognize and interact with antigenic determinants that are associated with class II human leukocyte antigen (HLA) molecules on the
surface of antigen-presenting cells. IL-1 is necessary for activation of T helper cells.

Haptens are small molecules that are not immunogenic on their own. Although antibodies can bind to haptens, the binding is usually below the threshold required to trigger an immune response. In order to make a hapten immunogenic, it must be conjugated to a carrier molecule. Additionally, haptens generally only have one epitope. Therefore, the statement "all of the above" is true as it encompasses all the given statements about haptens.

Hassall corpuscles are concentrically arranged accretions of epithelial reticular cells (derived
from endoderm) found only in the medulla of the thymus.

Without MHC class II, antigen presenting cells cannot present exogenously‐derived antigen to CD4
T cells, thus preventing a CD4 T cell response against the extracellular bacterium. Without surfacebound
antibody molecules, B cells cannot get activated and there would be no antibody production
against the antigen. Without antibody production, there would be diminished phagocytosis of the
antigen by phagocytes and no classical complement activation to eliminate the pathogen. Without Tolllike
receptors, macrophages and dendritic cells would have decreased recognition of the antigen;
consequently, there would be no killing by the macrophage and very little antigen presentation of the
antigen to CD4 T cells. Without the complement components, there would be reduced inflammation at
the site of infection, no direct killing of the pathogen via the complement pathway, and no opsonization
of the pathogen by complement components (reduced pathogen uptake by phagocytes).

T lymphocytes mature and become immunocompetent in the cortex of the thymus, whereas
B lymphocytes do so in the bone marrow.
After an antigenic challenge, lymphocytes proliferate and differentiate in various lymphoid tissues.

The membrane attack complex is formed by the activation of complement…this is a detail
about complement activation that I don’t expect you to know for now…

Antibody binding to antigen can trigger all of the events described in A‐D. Recall that T cells are
activated when they encounter their specific antigen presented in MHC class I or II by antigenpresenting
cells. While the B cell may become activated when surface‐bound antibody binds its specific
antigen and then go on to present the antigen to the T cell, the activation of the T cell is a consequence
of presentation of the antigen by the B cell, not a direct consequence antigen binding to antigen.

The immune response is decreased by T suppressor (Ts) cells. Their activity is thought to
help prevent autoimmune responses against self-antigens.

Epithelial reticular cells of the medulla congregate to form Hassall (thymic) corpuscles.