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Major histocompatibility complex class II molecules

Aguas, A., Esaguy, N., Sunkel, C.E., Silva, M.T. (1990). Cross-reactivity and sequence homology between the 65 kilodalton mycobacterial heat shock protein and human lactoferrin, transferrin, and DR beta subsets of major histocompatibility complex class II molecules. Infect. Immun. 58, 1461-1470. [Pg.450]

The staphylococcal superantigens initially bind to conserved elements on major histocompatibility complex class II molecules with relatively high affinity (A(i 10 mol 1 ). These receptors are found in abundance, throughout the body, on antigen-presenting cells such as macrophages and monocytes. However, each toxin... [Pg.160]

Cytokines, including tumour necrosis factor (TNF) and interferon-y, favour the secretion of numerous chemokines and the expression of adhesion molecules by endothelial cells. The mechanisms of action of the principle drugs used in MS, and in priority beta interferons, are the following (1) inhibition of the expression of major histocompatibility complex class II molecules, (2) inhibition of metal-loproteases, (3) induction of immunosuppressor cytokines. [Pg.703]

Hughes DA, Binder AC, Piper Z, Johnson IT, Lund EK. Fish oil supplementation inhibits the expression of major histocompatibility complex class II molecules and adhesion molecules on human monocytes. Am J Clin Nutr 1996 63 267-272. [Pg.58]

Nag, B Passmore, D Kendrick, T., Bhayani, H Sharma, S. D. (1992). N-linked oligosaccharides of murine major histocompatibility complex class II molecule. J. Biol. Chem. 267,22624-22629. [Pg.285]

Mehindate K, Thibodeau I, Dohlsten M, Kalland T, Sekaly RP, Mourad W Cross-linking of major histocompatibility complex class II molecules by staphylococcal enterotoxin A superantigen is a requirement for inflammatory cytokine gene expression. J Exp Med 1995 182 1573-1577. [Pg.21]

Fleischer B, Schrezenmeier H T cell stimulation by staphylococcal enterotoxins. Clonally variable response and requirement for major histocompatibility complex class II molecules on accessory or target cells. J Exp Med 1988 167 1697-1707. [Pg.179]

Stiles BG, Bavari S, Krakauer T, Ulrich RG. Toxicity of staphylococcal enterotoxins potentiated by lipopolysac-charide Major histocompatibility complex class II molecule dependency and cytokine release. Infect Immun. 1993 61 5333-5338. [Pg.629]

J. Hammer, C. Bolin, D. Papadopoulos, J. Walsky, J. Higelin, W. Danho, F. Sinigaglia, and Z. A. Nagy, High-affinity binding of shmt peptides to major histocompatibility complex class ii molecules by anchor combinations. Proc. Natl. Acad. Sci. 91, 4456 (1994). [Pg.457]

Family history of RA. Genetic studies demonstrate a strong correlation between RA and the presence of major histocompatibility complex class II human leukocyte antigens (HLA), specifically HLA-DR1 and HLA-DR4.4,5 HLA is a molecule associated with the presentation of antigens to T lymphocytes. [Pg.868]

Ironically, SE or TSST-1 concentrations that cause T-cell proliferation do not always correlate with receptor affinity. For instance, SEE binds HLA-DR with 100-fold lower affinity relative to the very similarly structured SEA however, SEE stimulates T-cell proliferation to equivalent levels as SEA. The dose-response curves for cytokine and chemokine production in vitro by staphylococcal superantigen-stimulated cells are also very similar despite differences in affmity/specificity for major histocompatibility complex class II and T-cell receptor V/3 molecules. Overall, these observations suggest that the biological effects of staphylococcal superantigens are induced at rather low, nonsaturating occupancy rates not readily classified by typical biokinetics. [Pg.163]

SEA (Leu-48-Gly) and SEB (Phe-44-Ser) mutants unable to bind major histocompatibility complex class II remain emetic but lack T-cell mitogenic effects. " A disulfide loop in SEs, which is absent in the non-enterotoxic TSST-1, may be responsible for the emetic activity of SEs but that too remains controversial. Carboxymethylation of histidines on SEA or SEB generates superantigenic molecules devoid of enter-otoxicity or skin reactivity. This chemically modified SEB also inhibits, perhaps in a competitive fashion, the... [Pg.164]

Kaneko Y, Kuwano K, Kunitake R, et al. Immunohistochemical localization of B7 costimulating molecules and major histocompatibility complex class II antigen in pulmonary sarcoidosis. Respiration 1999 66(4) 343-348. [Pg.181]

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. [Pg.739]

An unknown antigen presented by the major histocompatibility complex (MHC) class II molecules causes T cells to become autoreactive (Fig. 26-1). Once activated, T cells penetrate the... [Pg.432]


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Histocompatibility

Histocompatibility complex

Major histocompatibility

Major histocompatibility complex

Major histocompatibility complex (MHC class II molecule

Major histocompatibility complex class

Major histocompatibility molecules

Major histocompatibility, class

Major molecules

Molecules complex

Molecules, classes

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