Disease relevance of H2-Ob

• From the molecular characterization of the two hotspots located in the Eb gene and the Pb-Ob interval, it appeared that there are several common molecular elements, the consensus of the middle repetitive MT-family, TCTG or CCTG tetramer repeats, and the solitary long terminal repeat (LTR) of mouse retrovirus [1].
• The H2-Ab gene influences the severity of experimental allergic encephalomyelitis induced by proteolipoprotein peptide 103-116 [2].
• These granuloma macrophages (GR-Mphi) displayed dense Fc and C3 receptors, and about 50% expressed H-2I region-encoded determinants (Ia antigens) [3].
• It was shown that 46F/HA127-133/54A(18mer) peptide which was prepared by introducing hemagglutinin (HA)127-133 of influenza virus into the H-2Ab binding component induced significant T cell responses and antibodies (Ab) specific for HA127-133 in H-2Ab mice [4].

High impact information on H2-Ob

• The former cells are activated by a set of MHC gene products that are expressed mainly on immunological cells (H-2I-coded antigens), whereas the latter recognize a different set of MHC gene products that are expressed on almost all cells of the mouse (H-2K/D-coded antigens) [5].
• A previously unknown major histocompatibility complex class II molecule consisting of the beta chain encoded by the H-2Ob gene and an unknown alpha chain was recently described [6].
• Moreover, cross-reactive NP-induced CS responses could be transferred by NP-O-Su-primed lymph node cells from the AKR (Igh-1d) strain, into naive recipients homologous at the H-2D region, but only non-cross-reactive NP responses could be transferred into strains homologous at the H-2I region [7].
• These data are interpreted to suggest that the antigen is bound by cells of a clone functional helper T-cell hybridoma line in conjunction with products controlled by H-2I and that the receptor of these cells may have considerably higher affinity for Ia-associated than for regular antigen [8].
• Curiously, in marked contrast to the findings on CML responses in vitro, no evidence has been found that H-2I-restricted T-cells contribute to GVHD, either as effector cells or as helper cells [9].

Biological context of H2-Ob

• We conclude from these experiments that the same loci that cause acute skin graft rejection (H-2K, H-2D, and H-2I) are responsible for heart graft rejection [10].
• Description of the H-2K-, H-2I-, and H-2D-gene products of the H-2 haplotype [11].

Anatomical context of H2-Ob

• Recently, the H2-O heterodimer, encoded by H2-Oa and H2-Ob in the MHC class II region, has been shown to be physically associated with H2-M in B cells and to downregulate H2-M function [12].
• In nonprofessional APCs, e.g., L929 fibroblasts, IFN-gamma-inducible expression of the MHC class II-specific transcription factor CIITA is associated with coordinate expression of MHCII, Ii, H2-M, and H2-Oa genes but without concomitant H2-Ob induction [12].
• Regulatory mechanisms in cell-mediated immune responses. Role of I-J and I-C determinants in the activation of H-2I and H-2K/D alloantigen-specific suppressor T cells [13].
• T suppressor cells induced by either H-2K, H-2I or H-2D incompatible cells were found to be specific for the inducing alloantigen [14].
• These studies demonstrated that inflammatory GR-Mphi could function as antigen-presenting cells and that this accessory function was mediated by H-2I region gene products [3].

Associations of H2-Ob with chemical compounds

• Their binding to isolated H-2-Ab MHC glycoprotein as well as T-cell stimulatory capacity were assayed using a specific murine hybridoma T-cell line [38.H6], lymph node cells from the native 20-mer peptide primed C57BL/10 mice and human PBMCs from sensitised individuals [15].

Other interactions of H2-Ob

• Examination of H2-O expression in freshly isolated mouse organs revealed that H2-Oa- and H2-Ob-specific transcripts are present in both lymphoid and nonlymphoid tissues [12].
• Rfv-2 was located either in the H-2K or H-2I regions or in the Tla region [16].

Analytical, diagnostic and therapeutic context of H2-Ob

• Association of H2Ab with resistance to collagen-induced arthritis in H2-recombinant mouse strains: an allele associated with reduction of several apparently unrelated responses [17].

References