T cells classes

The two classes of MHC proteins are displayed on different cell types. Class I MHC proteins are found on almost all nucleated cells, including killer T cells. Class II MHC proteins are found mainly on cells involved in the immune response, including antigen-presenting cells, B cells, and T helper cells, but not T killer cells. 

CDS (homodimer or heterodimer) Ig cytotoxic T-cells class 1 MHC Adhesion to infected taiget cells... 

Antigen presentation can be viewed as an adaptation of an older cell-cell recognition function into two separate systems which identify distinct classes of MHC molecules. The first system has evolved to monitor and ensure the integrity of cell surface structures and consists of MHC molecules expressed on most cell types and mainly recognized by cytotoxic T cells (class 1 molecules). The second system has evolved to mediate cell-cell interactions in the immune response and consists of MHC molecules mostly expressed on macrophages and B cells and mainly recognized by regulatory T cells (class 11 molecules). The functional diversification between class I and class 11 molecules is reflected in substantial structural differences (see below). 

Figure 15.19 Schematic representation of the peptide-binding domain of a class I MHC protein. The al and a2 domains are viewed from the top of the molecule, showing the empty antigen-binding site as well as the surface that is contacted by a T-cell receptor. (Adapted from P.J. Bjdrkman et al.. Nature 329 506-512, 1987.)...

To date, there has not been a reported structure determination of a class 11 MHC-peptide-TCR complex. However, T-cell receptors that recognize class... 

Class 1 and class II MHC molecules bind peptide antigens and present them at the cell surface for interaction with receptors on T cells. The extracellular portion of these molecules consists of a peptide-binding domain formed by two helical regions on top of an eight-stranded antiparallel p sheet, separated from the membrane by two lower domains with immunoglobulin folds. These domains are differently disposed between the two protein subunits in class I and class II molecules. 

The antiinflammatory effects of statins likely result from their ability to inhibit the formation of mevalonic acid. Downstream products of this molecule include not only the end product, cholesterol, but also several isoprenoid intermediates that covalently modify ( pre-nylate ) certain key intracellular signaling molecules. Statin treatment reduces leukocyte adhesion, accumulation of macrophages, MMPs, tissue factor, and other proinflammatory mediators. By acting on the MHC class II transactivator (CIITA), statins also interfere with antigen presentation and subsequent T-cell activation. Statin treatment can also limit platelet activation in some assays as well. All these results support the concept that in addition to their favorable effect on the lipid profile, statins can also exert an array of antiinflammatory and immunomodulatory actions. 

COPD is a chronic inflammatory disease that results from prolonged and repeated inhalation of particles and gases, chronic (or latent) infection or an interaction of these factors. In many cases, the inflammation persists even when the exposure (in most cases smoking) is stopped. Prominent among the infiltrating leukocytes are neutrophils, CD8+ lymphocytes (Co-receptor for the T-cell receptor. CD8+ is specific for the class IMHC protein. It is expressed on the surface of cytotoxic T-cells and natural killer cells.) and CD68+ monocytic cells (A lysosomal antigen. All cells that rich in... 

IFN- 3 reduces the induction by inflammatory cytokines of adhesion molecules and of MHC class I and II complex on endothelial cells, a process preceding attachment and transendothelial migration of T-cells. These anti-inflammatory effects of IFN- 3 exemplify antagonistic actions of type I and type IIIFN. There is, indeed, much clinical evidence for the involvement of IFN-y in inflammatory processes - through activation of iNOS and subsequent secretion of NO - leading to the establishment of autoimmune diseases as for instance in rheumatoid arthritis. 

Group of transmembrane proteins engaged in the presentation of small peptide fragments to T-cells. Two classes of Major histocompatibility complex (MHC) molecules exist both of which are encoded by a highly polymorphic gene cluster. MHC class I and class II proteins present peptide fragments to CD8+ and CD4+ T-cells, respectively. The human MHC is also known as HLA, the murine MHC as H-2 complex. 

Class IIHLA molecules are expressed on the surface of antigen-presenting cells. They play a key role in presentation of processed linear peptide antigens of at least nine amino acids to T cells. Antigen is bound to the HLA antigen binding cleft formed by the a and 3 chains of the HLA class II molecule. This tri-molecular HLA-antigen complex binds in turn to the variable portion of the T-cell receptor. 

Bacterial or viral proteins linking T-cell receptors and MHC molecules through simultaneous interaction with the constant domains of all MHC class II molecules and of T-cell receptor (3-chains. Hence, superantigens are polyclonal T-cell activators most likely involved in the development of autoimmune diseases. 

The activation of DRF-3 through the TREF dependent pathway allows for chemokines such as RANTES to be produced. It also leads to the production of DFN-a and EFN-(3, which are involved in anti-viral immunity. The TREF pathway, activated by either TLR-3 or TLR-4, can also induce MHC class-II expression and costimulatory molecules, thus leading to T-cell activation. This provides an important link between innate and adaptive immunity. 

Based on the predicted effects on HIV-1 and T cell dynamics, antiviral genes have been grouped into three classes (Fig. 1) (von Laer et al. 2006b). Early inhibitors are classified as class 1, inhibitors of intracellular reproduction of the viral genome and production of viral gene product are class II, and late inhibitors are considered class 111. A comprehensive list of types of antiviral genes reported to date for each class is found in Table 1 (von Laer et al. 2006a). 

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