H-2 Class I Mouse, anti-Mouse, R718, Clone: M1/42, BD OptiBuild™

Description

• The M1/42 monoclonal antibody (mAb) specifically recognizes intact Histocompatibility-2 Region (H-2) class I antigens (Ags), also known as mouse Major Histocompatibility Complex class I (MHC-I) Ags
• This mAb reportedly binds to one or more of the H-2 Ags (H-2K, H-2D, and likely H-2L) that are primarily expressed on most nucleated somatic cells of hematopoietic and nonhematopoietic origin
• H-2 class I molecules are comprised of a ∼45-50 kDa type I transmembrane heavy chain glycoprotein that is noncovalently linked to ∼13 kDa β2-microglobulin (β2-m)
• The extracellular region of the polymorphic heavy chains is comprised of three globular domains (α1, α2, and α3), followed by a transmembrane region and a cytoplasmic tail
• Sequence variations are manifest in regions of the α1 and α2 domains that line the peptide-binding cleft involved in Ag presentation
• The M1/42 mAb reportedly binds to H-2 class I Ags from multiple mouse haplotypes including a, b, d, j, k, s, and u
• It does not bind to separated H-2 class I heavy chains or β2-m
• Cell surface CD8 molecules bind to invariant sites of the H-2 heavy chains and can provide coreceptor signaling for Ag-mediated activation through the T cell receptor
• H-2 class I molecules that present self-Ags can lead to self-tolerance of maturing CD8+ T cells due to thymic selection
• Alternatively, these molecules can present foreign peptide Ags to mature peripheral CD8+ T cells resulting in cell-mediated immune responses against foreign Ags
• H-2 class I Ags also serve as ligands for activating and inhibitory receptors expressed by NK cells and some T cells
• The M1/42 antibody is useful for analyzing H-2 class I Ag expression on cells or cell lines
• Cells from different experimental systems, eg, stressed cells that have undergone infection or transformation, may express little or no H-2 class I Ag
• In contrast, cells undergoing activation or responding to certain factors (eg, interferons) may express upregulated levels of these Ags.