Disease relevance of Graft vs Host Reaction

• The induction of graft vs host reaction in mice that carry both a rearranged B cell Ag receptors specific for hen egg lysozyme and expressing chronically circulating hen egg lysozyme Ag resulted in induction of high and sustained levels of circulating anti-hen egg lysozyme autoantibodies and glomerulonephritis with proteinuria [1].
• An overproduction of proinflammatory cytokines mediates the damaging sequelae of inflammation in pathologic conditions such as rheumatoid arthritis, graft-vs-host reaction, cachexia, and sepsis syndrome [2].

High impact information on Graft vs Host Reaction

• We previously have observed that T dependent immune functions were deficient for several months after induction of acute suppressive graft-vs-host-reaction (GVHR) by injection of parental C57BL/10 donor spleen cells into unirradiated (B10 x B10.BR) F, hosts [3].
• The mechanisms of the suppressive activity of spleen cells from mice undergoing a graft-vs-host reaction (GVH) to non-H-2 histocompatibility Ag were investigated [4].
• Alterations in the expression of colony-stimulating factor-1 and its receptor during an acute graft-vs-host reaction in mice [5].
• The splenic CSF-1-receptor bearing cells were in a Mac-1+ fraction that is consistent with a role for CSF-1 in the generation of host-derived splenic macrophages in acute graft-vs-host reaction [5].
• Modulation of F1 cytotoxic potentials by graft-vs-host reaction. Cooperative non-H-2- and H-2D region-gene control of F1 natural resistance to graft-vs-host reaction-associated immunosuppression [6].

Anatomical context of Graft vs Host Reaction

• B cell and Th cell functions were assessed in mice undergoing a graft-vs-host reaction (GvHR) in response to minor histocompatibility Ag by using the plaque-forming cell (PFC) response to the T-independent Ag TNP-Brucella abortus and the T-dependent Ag TNP-SRBC [7].
• Phenotypic characterization of cells from the peak proliferative time of the graft-vs-host reaction (C57BL/6J lymph node cells----irradiated LP/J, days 5-7) revealed the alpha ASGM1 and alpha Thy 1.2 identified cells with an approximate 80% concordance and that NK-1.1 staining was negligible [8].
• Stimulation in mixed lymphocyte culture reaction (MLR) or graft vs host reaction has been shown to be governed by genes located in the I-region (immune response region) of the H-2 complex in mice (Bach et al. 1972 and Klein and Park 1973) and it appears that the H-2K and H-2D regions play only a minor role in that reaction [9].

Associations of Graft vs Host Reaction with chemical compounds

• LEW rats received a lethal dose (35 mg/kg) of busulfan followed by injection of 1 x 10(8) (CAP x LEW) F1 marrow cells, which are unable to induce a graft vs host reaction in LEW recipients [10].
• At much higher doses (50-200 mg/kg) ADA 202-718 enhanced the local graft-vs-host reaction in the rat [11].
• Moreover, LF 1695 was tested in vivo in the experimental graft vs host reaction (GvHR) in mice [12].
• Prevention of graft-vs-host reaction induced immunodeficiency by treatment with splenopentin (DAc-SP5) [13].
• Effect of FK 506 in combination with prednisolone on the graft-vs-host reaction after small bowel transplantation in rats [14].

Gene context of Graft vs Host Reaction

• Interleukin 2 receptor dysfunction in mice undergoing a graft-vs-host reaction [15].
• We explored the immunoincompetence of mice undergoing a chronic graft-vs-host reaction (GVHR) across minor histocompatibility barriers [16].
• Partial reconstitution of TNP-Ficoll responses and IgG3 expression in Xid mice undergoing graft-vs-host reaction [17].
• Another possibility is that the reactive metabolite directly alters the class II MHC molecule leading to a graft-vs-host reaction [18].

Analytical, diagnostic and therapeutic context of Graft vs Host Reaction

• Our previous study revealed that in F1 mice raised by crossing C3H/He or AKR/J mice with various H-2-congenic B10-series strains, parental H-2k spleen cells (SC) could not induce the graft-vs-host reaction (GvHR)-associated immunosuppression (GAIS) [6].
• Donor pretreatment with deoxyspergualin on prevention of graft-vs-host reaction after small bowel transplantation [19].

References