Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.1.1.148 (Thy1)
 1,210 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A nonlethal conditioning regimen involving administration of mAb in vivo, low-dose WBI and 700 rads of thymic irradiation, permits engraftment of T cell-depleted allogeneic BM. Engraftment of class I + II disparate allogeneic BM after conditioning with this regimen required depletion of both L3T4 and Lyt2 host T cell subsets in vivo. Treatment with a combination of specific mAbs to each subset (GK1.5 plus 2.43) was more effective than treatment with an anti-Thy1 mAb (30-H12). The low incidence of engraftment after 30-H12 treatment is probably due to reduced efficiency of 30-H12 in depletion of host alloreactive cell populations rather than an effect of this mAb on a particular population of donor cells that are important for engraftment.
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PMID:Engraftment of allogeneic bone marrow following administration of anti-T cell monoclonal antibodies and low-dose irradiation. 265 Jan 9

Cells required for the in vitro generation of syngeneic cytotoxic T-lymphocytes (CTL) against the P815 mastocytoma in the DBA/2 mouse strain were investigated. For both immune and tumor-bearing host spleen cells, CTL effector cells were eliminated by treatment with anti-Thy1.2, anti-Lyt1.1, or anti-Lyt2.1 and C', but were resistant to anti-L3T4 (GK1.5). Thus, CTL effectors (and their precursors) were Lyt1+2+, L3T4-. However, P815-specific CTL could not be generated in the absence of L3T4+ cells, whose function could be replaced with exogenous interleukin-2 (IL-2). When monoclonal antibodies against L3T4 were added to mixed leukocyte tumor cultures, CTL generation was markedly inhibited. Depletion of accessory cells also led to a marked reduction in CTL generation, which could be restored to control levels by adding adherent cells from normal spleens or with exogenous IL-2, but not with IL-1. Thus, accessory cells are apparently required to present the tumor antigens of this Ia-negative tumor to T-helper cells.
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PMID:Phenotype of syngeneic tumor-specific cytotoxic T-lymphocytes and requirements for their in vitro generation from tumor-bearing host and immune spleens. 296 66

We previously demonstrated that Thy1.2+, CD4+, Ia-T cells are responsible for transfer of adoptive murine experimental hypersensitivity pneumonitis (adoptive EHP). To characterize the cells responsible for development of pulmonary inflammation in the recipient animals, we depleted recipients of CD4+ cells using monoclonal antibody GK1.5 before administration of Micropolyspora faeni-sensitized cultured C3H/HeJ spleen cells (SC) and intratracheal (i.t.) challenge with M. faeni. We also used the same depletion technique to determine the contribution of these cells to the pulmonary response to i.t. M. faeni in animals that did not receive cultured cells (direct EHP). The nature and extent of pulmonary inflammatory changes in these animals were assayed either 4 days after i.t. challenge with M. faeni in adoptive EHP or 2 days after i.t. challenge with M. faeni in direct EHP. Cultured M. faeni-sensitized SC could transfer EHP to naive animals or those treated with an irrelevant antibody. Depletion of CD4+ cells ablated the ability of recipient animals to express adoptive EHP. Two days after i.t. M. faeni (direct EHP), there was extensive neutrophilic infiltration of the lung that was not affected by depletion of CD4+ cells. We conclude that the ability to express adoptive EHP is dependent on the presence of CD4+ cells. In contrast, the acute inflammatory response to M. faeni is not CD4+ cell dependent.
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PMID:Experimental hypersensitivity pneumonitis. Effect of CD4 cell depletion. 790 6