mhc class i molecules presents peptides to t cells and is only found on specific types of nucleated cells.
mhc class i molecules presents peptides to t cells and is only found on specific types of nucleated cells.
presents peptides to t cells and is only found on specific types of nucleated cells?
mhc class i molecules
section::::types of t cell.:conventional adaptive t cells.:cytotoxic cd8+ t cells.









































cytotoxic t cells (t cells, ctls, t-killer cells, killer t cells) destroy virus-infected cells and tumor cells, and are also implicated in transplant rejection. these cells are defined by the expression of cd8 on the cell surface. these cells recognize their targets by binding to short peptides (8-11aa) associated with mhc class i molecules, present on the surface of all nucleated cells. cd8+ t cells also produce the key cytokines il-2 and ifnγ, which influence the effector functions of other cells, in particular macrophages and nk cells.
t cell
drugs can cause scars by subverting the antigen presentation pathways which recognize and trigger immune responses to non-self epitopes (i.e. antigens) on foreign proteins. these proteins are taken up by antigen-presenting cells (apc) and degraded into small peptides. the peptides are inserted into a groove on hla proteins that are part of major histocompatibility complexes (i.e. mhc) and presented to t cell receptors (tcr) on nearby cytotoxic t cells (i.e. cd8 t cells) or t helper cells (i.e. cd4 t cells). t cell receptors are heterologous; only a small fraction of them can bind a particular epitope on presented peptides and this binding is restricted to non-self epitopes. upon binding a non-self epitope on a presented peptide, a t cell receptor becomes active in stimulating its parent cell to mount one of two types of immune responses based on whether the apc presenting the peptide is professional or non-professional in type. non-professional apc include all nucleated cells; these cells load the processed peptides onto mhc class i (i.e. hla-a, hla-b, or hla-c) proteins and thereon present the peptides to cd8 t cells. those cd8 t cells whose t cell receptors bind an non-self epitope on the peptides are stimulated to attack cells or pathogens expressing this epitope. professional apc are dendritic cells, macrophages, and b cells. they load processed peptides onto mhc class ii (i.e. hla-dm, hla-do, hla-dp, hla-dq, or hla-dr) proteins and thereon present the peptides to cd4 t cells. those cd4 t cells whose t cell receptors bind a non-self epitope on presented peptides are stimulated to orchestrate various immune reactions that attack soluble proteins, pathogens, and host cells and tissues that express the non-self epitope. scars-inducing drugs can act through these pathways to cause cd8 or cd4 t cells to mount immune responses that are inappropriately directed against bodily tissues. four models propose the underlying mechanisms by which scars-inducing drugs may activate t cells to mount immune responses against self:
severe cutaneous adverse reactions