At first glance, it would seem a dangerous strategyfor the thymus to actively promote the survival, matura-tion, and emigration of developing T cells that bind weaklyto self peptides bound to self MHC molecules. Would itnot be safer to get rid of these T cells, along with those thatbind strongly to such self-peptide–MHC complexes, as thiswould seem a more secure way to avoid autoimmune reac-tions?

At first glance, it would seem a dangerous strategyfor the thymus to actively promote the survival, matura-tion, and emigration of developing T cells that bind weaklyto self peptides bound to self MHC molecules. Would itnot be safer to get rid of these T cells, along with those thatbind strongly to such self-peptide–MHC complexes, as thiswould seem a more secure way to avoid autoimmune reac-tions?

Human Physiology: From Cells to Systems (MindTap Course List)

9th Edition

ISBN:9781285866932

Author:Lauralee Sherwood

Publisher:Lauralee Sherwood

Chapter12: Body Defenses

Section12.4: B Lymphocytes: Antibody-mediated Immunity

Problem 3CYU

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Similar questions

Why is it necessary for immature T lymphocytes toundergo a two-step selection process through whichantigen-reactive cells are first selected followed bythe elimination of cells that react strongly withself-antigens?
Some primitive organisms, such as invertebrates, have no lymphocytes and thus lack an adaptive immune system, but they have somecomponents of an innate immune system, including phagocytes andcertain protective proteins. What are some general features of innateimmunity that make it very valuable to organisms lacking more specific antibody- and cell-mediated responses? What are some disadvantages to having only an innate immune system?
To avoid the potential for activating self-reactive T cells that might cause autoimmunity, naive T cell activation has stringent requirements for co-stimulatory signals in addition to the engagement of T-cell receptors with peptide: MHC complexes. Yet this requirement is abandoned once T cells have differentiated into effector cells. Name two effector T cell functions that would fail if effector T cells also required T-cell receptor signals plus co-stimulatory signals through CD28 to elicit their effector responses.
How is the newly emerging repertoire of T cells, with their diverse pre-TCRs, further differentiated so that a productive interaction with self-MHC–peptide complexes can occur?
Which statements are true? Explain why or why not.1 T cells whose receptors strongly bind a self-pep-tide–MHC complex are killed off in peripheral lymphoidorgans when they encounter the self peptide on an anti-gen-presenting dendritic cell. 2 To guarantee that the antigen-presenting cells inthe thymus will display a complete repertoire of self pep-tides to allow elimination of self-reactive T cells, the thy-mus recruits dendritic cells from all over the body. 3 The antibody diversity created by the combinato-rial joining of V, D, and J segments by V(D)J recombinationpales in comparison to the enormous diversity created bythe random gain and loss of nucleotides at V, D, and J join-ing sites.
In a mixed lymphocyte reaction, T cells from individual A make a robust response to antigen-presenting-cells from individual B, as long as the two individuals express different alleles of MHC molecules. Estimates indicate that up to 10% of the T cells from individual A may contribute to this response. If one performed this assay using responder T cells from a child and antigen-presenting cells from one parent, the result would be: A massive proliferative response made by the antigen-presenting cells of the parent A very weak response by the child’s T cells, involving only 0.1% of their T cells The complete absence of any proliferative response by the child’s T cells A robust cytolytic response that kills all of the parent’s antigen-presenting cells A robust response by the child’s T cells
In regard to antigen presentation, MHC class I molecules usually present peptides derived from _____, whereas MHC class II molecules usually present peptides derived from _____. a. intracellular cytosolic sources; vesicular system b. phagolysosome; proteasomes c. MIIC; self proteins d. CLIP; HLA-DM e. endocytic vesicles; endoplasmic reticulum.
Describe the basic structure of class I and class IImajor histocompatibility complex (MHC) proteins. Inwhat functional ways do they differ?
Why is it that Rh incompatibility can be a serious problem when anRh-negative mother is carrying an Rh-positive fetus, but ABOincompatibility between mother and fetus is usually no problem?That is, a type A mother can usually safely carry a type B fetus.(Hint: The antibodies produced by an Rh-negative mother againstthe Rh antigen are usually IgG, whereas the antibodies producedagainst the A or B antigens are IgM.) Because the Rh antigenobviously serves no vital function (most humans lack it), why do youthink it hasn’t been completely eliminated during human evolution?
MHC restriction is best described as a. elimination of thymocytes bearing T-cell receptors that are unable to interact with self-MHC molecules b. preferential survival and proliferation of thymocyes that survive negative selection c. T-cell recognition of a peptide antigen only when it is bound to a particular form of MHC molecule d. a state of non-responsiveness to a peptide antigen e. a condition in which either MHC class I or class II molecules are not expressed on cells.
Clonal selection therefore requires a mechanism for producing a great diversity of antibodies. How is this diversity achieved?
One striking feature of TCR interactions with peptide:MHC complexes is that amino acid residues in the MHC protein are as important to the TCR binding strength as are amino acid residues in the pathogen-derived peptide. This feature is in contrast to antigen recognition by antibodies, which is a direct interaction that is independent of other host proteins. Based on the different functions of T cells versus antibodies in the adaptive immune response, the fact that TCRs recognize components of both the MHC and the bound peptide exists to: Prevent TCRs from binding only to surface exposed epitopes of native pathogens Prevent immune evasion by a pathogen that has mutated the sequences required for antibody recognition Put constraints on T cell recognition, due to the potentially damaging effector molecules made by activated T cells Ensure that TCRs are focused on recognizing antigens associated with host cells, and not those that are free in solution Ensure that the pathogen has already…