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Chapter 12 : T-Cell-Mediated Cytotoxicity

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Abstract:

Cell-mediated reactions feature infiltrations of tissues by mononuclear cells (lymphocytes and macrophages). The importance of cell-mediated immunity (CMI) in infectious diseases has been brought to the forefront by the variety and number of opportunistic infections with viruses, protozoa, fungi, and mycobacteria in AIDS patients who have defective T-cell-mediated immunity. Cytotoxic T (TCTL) cells lyse or “kill” target cells expressing specific antigens in vitro; T cells that mediate delayed-type hypersensitivity (TDTH) cells release “lymphokines” with biologic activity after reaction with specific antigens in vitro. Major histocompatibility complex (MHC) restriction is mediated by the receptors of T cells, which contain recognition sites for both antigens and MHC molecules. Natural killer (NK) cells are related to TCTL cells but do not require antigenic stimulation for generation. The first appreciation of T-cytotoxic activity came from the recognition that TCTL cells could "kill" specific target cells in vitro. The major cellular infiltrate in the epithelial cells is made up of CD8+ cells; CD4+ cells are seen in the interstitial connective tissues. The major limitation to the clinical application of solid organ transplantation is the availability of donor organs. Examples of TCTL-cell-mediated reactions presented in this chapter include contact dermatitis, viral exanthems (smallpox), tissue graft rejections, and autoimmune diseases, such as thyroiditis.

Citation: Sell S. 2001. T-Cell-Mediated Cytotoxicity, p 401-430. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch12
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Figures

Image of Figure 12.1
Figure 12.1

Two pathways of TCTL cell killing of target cells. TCTL cell killing is mediated through endogenous proteases (capases) in the target cell. Upon binding of the TCTL-cell receptor (TCR) to antigen of the class I MHC of the target cells, TCTL cells activate two killing systems: Fas ligand and granule exocytosis (perforin and granzymes). Fas ligand on the T cells contains an intracellular “death domain” that binds to at least five intracellular signaling molecules. This activates JUN kinases (JNK) and capase 8. These in turn activate a series of downstream capases. Perforin reacts with the target cell membrane to produce “holes” in the membrane, permitting granzymes to enter the target cell. Upon entering the cytoplasm, granzymes also activate downstream capases. The active capases act on a variety of substrates, including but not limited to structural proteins (laminin, G-actin, etc.), kinases, cell cycle-controlling proteins (Rb and mdm-2), and DNA. This latter action results in the fragmentation of DNA characteristic of apoptosis.

Citation: Sell S. 2001. T-Cell-Mediated Cytotoxicity, p 401-430. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch12
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Image of Figure 12.2
Figure 12.2

Summary of factors determining selection of immune effector systems. Selection of which immune effector mechanisms will predominate after an immune response depends on the location of the antigen-presenting cell (follicular or parafollicular), the type of antigen processing (endogenous or exogenous), the class of MHC-associated antigen presentation, the presence of accessory cells (mast cells, NK cells, etc.), the cytokines produced, and the population of T-helper cells activated. Exogenous antigen presentation by professional antigen-presenting cells (dendritic or follicular cells) leads to activation of Th1 or Th2 cells and stimulation of antibody production. In this figure, it is postulated that separation of Th1 activation from helping B cells make antibody to differentiation into TDTH cells, which mediate delayed-type hypersensitivity, is dependent on the nature of the antigen-presenting cells. Procession of antigen by dendritic or follicular antigen-presenting cells leads to activation of Th1 helper cells; processing by parafollicular interdigitating reticulum cells stimulates Th1 cells to become effector cells for delayed-type hypersensitivity. Endogenous processing of antigen by nonprofessional antigen-presenting cells results in presentation by class I MHC to CD8+ precursors of TCTL cells. TCTL cells recognize antigens on surfaces of other cells and produce molecules (granzymes or perforins) that kill the target cells. TDTH cells release lymphokines, which act through macrophages to effect delayed-type hypersensitivity reactions.

Citation: Sell S. 2001. T-Cell-Mediated Cytotoxicity, p 401-430. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch12
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Image of Figure 12.3
Figure 12.3

Reaction of sensitized lymphocytes with target cells in vitro. T lymphocytes from a sensitized donor infiltrate and surround monolayer target cells, seemingly without effect on viability or morphologic appearance of target cells. As a result of this infiltration, monolayer cells become separated from each other and from the culture surface. Monolayer cells that retain contact with the monolayer remain viable, but when separated from other monolayer cells, morphologic changes consistent with cell death occur. These alterations do not occur in tissue culture cells that become separated from the monolayer in the presence of normal lymphocytes. Fluids and washings taken from monolayers treated with sensitized lymphocytes cannot be used to initiate new cultures, whereas fluids or washings of cultures treated with normal lymphocytes can. (Modified from P. Biberfield, G. Holm, and P. Perlmann, Exp. Cell Res. 52:672, 1968. Copyright Academic Press.)

Citation: Sell S. 2001. T-Cell-Mediated Cytotoxicity, p 401-430. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch12
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Image of Figure 12.4
Figure 12.4

Reaction of sensitized lymphocytes with target cells in vivo (morphologic changes in experimental renal graft rejection or allergic thyroiditis). Changes similar to those observed in reactions of sensitized lymphocytes with tissue culture monolayers occur during renal homograft rejection or with thyroid follicle-lining cells in allergic thyroiditis. Mononuclear cells appear first in perivenular areas and then invade stroma of organ. Invasion of tubules or follicles follows. Lymphocytes appear to pass through basement membrane, separating renal tubule or thyroid follicle-lining cells from basement membrane and from other follicular cells. Death of lining cells occurs when these cells are isolated from basement membrane and from other tubule or follicular cells. (Modified from M. H. Flax, Lab. Investig. 12:199, 1963.)

Citation: Sell S. 2001. T-Cell-Mediated Cytotoxicity, p 401-430. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch12
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Image of Figure 12.5
Figure 12.5

Evolution of contact dermatitis reaction. A contact-sensitizing hapten such as dinitrophenol or poison ivy oleoresin needs to be in either a lipid-solvent or lipid-soluble form to penetrate the epidermis. In so doing, the contact-sensitizing hapten joins to host proteins to become a complete antigen. In a sensitive individual, penetration of the epidermis brings the antigen into contact with specifically sensitized TCTL cells that react with the antigen and initiate a cell-mediated reaction that destroys the epithelial cells.

Citation: Sell S. 2001. T-Cell-Mediated Cytotoxicity, p 401-430. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch12
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Image of Figure 12.6
Figure 12.6

Stages of skin graft rejection. The type of rejection of an allogeneic skin graft depends upon immune reactivity. An autograft or synograft will “take,” that is, survive and heal into the grafted site. An allograft to an unsensitized individual will be rejected after a stage of vascularization by a mononuclear cell infiltrate. An allograft to a sensitized recipient will not become vascularized and will be rejected by ischemic necrosis within a few days after transplantation. (See text for details.)

Citation: Sell S. 2001. T-Cell-Mediated Cytotoxicity, p 401-430. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch12
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Image of Figure 12.7
Figure 12.7

Some fates of human renal allografts. Renal allografts are subject to immune rejection as well as to recurrence of the original disease. Long-term uncomplicated survival essentially only occurs with completely matched donor and recipient, such as with identical twins. Immune rejection may be caused by either antibody or cell-mediated reactions. Immediate rejection is caused by reaction of preformed antibody with vascular endothelium and activation of the clotting system. Acute rejection is caused mainly by mononuclear cell infiltration (TCTL-cell-mediated tubulitis). Chronic rejection occurs as a result of continuing low-grade endarteritis because of long-term deposition of antibody or immune complexes. Recurrence of the original disease may occur if the predisposing cause is not controlled. Anti-GBM, anti-glomerular basement membrane.

Citation: Sell S. 2001. T-Cell-Mediated Cytotoxicity, p 401-430. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch12
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Image of Figure 12.8
Figure 12.8

Vaccination against smallpox. Introduction of vaccinia virus into the skin results in proliferation of organisms in epithelial cells followed by development of TCTL cells and destruction of infected cells. Viral antigens are carried by lymphatics to draining lymph nodes, where primary T-cell response results in production of sensitized cells. The sensitized cells return to attack virus-infected epithelial cells, producing a take, i.e., a necrotic delayed skin reaction. The take reaction indicates establishment of protective immunity to reinfection.

Citation: Sell S. 2001. T-Cell-Mediated Cytotoxicity, p 401-430. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch12
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Image of Figure 12.9
Figure 12.9

Antigen, antibody, and immune response during the course of hepatitis B virus infection. Within 2 months after infection, systemic symptoms and jaundice are associated with the presence of hepatitis B virus DNA and hepatitis B virus antigens in the blood and elevations of alanine aminotransaminase, which is an indicator of liver cell injury. Antibodies to HBc (core) antigens appear at about the same time. Anti-HBsAg may not become elevated until 6 months after the initial infection. Failure to produce anti-HBsAg is associated with a prolonged carrier state and continued production of infectious virus.

Citation: Sell S. 2001. T-Cell-Mediated Cytotoxicity, p 401-430. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch12
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Image of Figure 12.10
Figure 12.10

Evolution of experimental allergic thyroiditis. The lesions begin as perivascular infiltrates that extend through the interfollicular stroma to invade the follicular lining cells. Destruction of the lining cells occurs wherever mononuclear cells invade. Before destruction, the lining cells may enlarge and become more densely stained in histologic sections (Hurthle or Askanazy cells). After the follicular lining cells are destroyed, the follicles may be filled with mononuclear cells (Askanazy body). In experimental allergic thyroiditis, the lesions always resolve, presumably because of regeneration of the follicular lining cells similar to that of epithelial cells after contact dermatitis.

Citation: Sell S. 2001. T-Cell-Mediated Cytotoxicity, p 401-430. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch12
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Tables

Generic image for table
Table 12.1

A brief history of clinical transplantation

Citation: Sell S. 2001. T-Cell-Mediated Cytotoxicity, p 401-430. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch12
Generic image for table
Table 12.2

Stages of renal allograft rejection a

Citation: Sell S. 2001. T-Cell-Mediated Cytotoxicity, p 401-430. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch12
Generic image for table
Table 12.3

Methods used to evaluate transplant function or rejection a

Citation: Sell S. 2001. T-Cell-Mediated Cytotoxicity, p 401-430. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch12
Generic image for table
Table 12.4

Survival rates for transplanted solid organs

Citation: Sell S. 2001. T-Cell-Mediated Cytotoxicity, p 401-430. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch12
Generic image for table
Table 12.5

Possible mechanisms of tolerance of the fetus as a homograft

Citation: Sell S. 2001. T-Cell-Mediated Cytotoxicity, p 401-430. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch12
Generic image for table
Table 12.6

Hepatitis viruses a

Citation: Sell S. 2001. T-Cell-Mediated Cytotoxicity, p 401-430. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch12
Generic image for table
Table 12.7

Relation of cell-mediated experimental autoimmune diseases to human diseases a

Citation: Sell S. 2001. T-Cell-Mediated Cytotoxicity, p 401-430. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch12

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