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J W Moorhead

Publications and source records attributed to J W Moorhead.

At least 19 recordsLinked to original sources
PubMed1979

Soluble factors in tolerance and contact sensitivity to 2,4-dinitrofluorobenzene in mice. III. Histocompatibility antigens associated with the hapten dinitrophenol serve as target molecules on 2,4-dinitrofluorobenzene-immune T cells for soluble suppressor factor.

Previous studies have shown that suppression of 2,4-dinitrofluorobenzene (DNFB) contact sensitivity by soluble suppressor factor (SSF) requires that the donor of immune lymph node (LN) cells and of SSF share either the H-2K and/or H-2D region of the major histocompatibility complex. Thus, target or acceptor molecules for SSF appear to be coded for by genes within the H-2K and H-2D loci. Experiments were done to investigate the nature of these target molecules and to determine what cell types expressed them. It was found that purified lymph node T cells are suppressed by SSF indicating that T cells express the acceptor molecules. Adsorption experiments showed that the only cells capable of adsorbing the suppressor factor are DNFB-immune T cells from donors which share with the factor-producing strain either the H-2K or H-2D locus. This adsorption can be specifically blocked by pretreating the immune LN cells with antibodies directed against H-2K and/or H-2D determinants or against the hapten DNP but not by antibodies against Ia or theta-antigens. Collectively, these results indicate that the target molecules are expressed only by DNFB-immune T cells and are comprised of histocompatibility antigens associated with DNP.

Animals↗
PubMed1979

Active suppression of 1-fluoro-2,4-dinitrobenzene-immune T cells. Requirement of an auxiliary T cell induced by antigen.

We investigated T-T cell interactions in the suppression of contact sensitivity. Suppressor cells that block the efferent limb of sensitivity (Ts-eff) can inhibit the passive transfer of contact sensitivity mediated by 1-fluoro-2,4-dinitrobenzene immune cells (T DH). But, Ts-eff cannot block the passive transfer of TDH which comes from cyclophosphamide (Cy) pretreated sensitized mice. We interpret these results to indicate that lymph node cells from sensitized mice contain not only TDH but also another intermediate cell which is required for the suppression of TDH by Ts-eff. This intermediate cell is sensitive to cyclophosphamide and requires antigen activation for its development. It is sensitive to adult thymectomy and anti-brain associated theta serum and is therefore designated as an auxiliary T-suppressor cell (Ts-aux). It is not sensitive to splenectomy and it carries I-J determinants. Ts-aux are required for the activity of suppressors of the efferent limb (Ts-eff) but not of suppressors of the afferent limb (Ts-aff). Thus, in the feedback loops in contact sensitivity, the generation of Tdh is coordinated with the development of auxiliary Ts which are essential for the suppression of those TDH.

Animals↗
PubMed1978

Subpopulations of mouse T lymphocytes. II. Suppression of graft-vs.-host reactions by naturally proliferating splenic T cells.

The immunological role of a naturally proliferating subpopulation of splenic T cells was investigated using the graft-vs.-host (GvH) reaction on the mouse. Normal parental spleen cells, purified splenic T cells or lymph node cells were pulse-treated for one hour in vitro with tritiated thymidine of high specific activity ([3H]dThd, "thymidine suicide"). The treatment specifically and selectively kills proliferating cells which are actively synthesizing DNA, i.e. cells in S phase. Following treatment, the cells were transferred to F1 recipients and the GvH reaction measured by the splenomegaly assay. The results showed that the GvH effector cells in the donor spleen and lymph node are nonproliferating T cells. Furthermore, donor spleen cells treated with [3H]dThd consistently had enhanced GvH reactivity when compared to the controls, while the phytohemagglutinin response of these same treated cell suspensions was significantly inhibited. When purified splenic T cells were used, treatment with [3H]dThd also caused an increase in the GvH reaction, showing that a T cell population was being affected by the cycleactive agent. These results indicated that some naturally proliferating T cells have suppressor functions, and their specific inactivation allows nonproliferating effector T cells to mount a more vigourous GvH reaction.

Animals↗
PubMed1977

Soluble factors in tolerance and contact sensitivity to 2,4-dinitrofluorobenzene in mice. I. Suppression of contact sensitivity by soluble suppressor factor released in vitro by lymph node cell populations containing specific suppressor cells.

Tolerance to 2,4-dinitrofluorobenzene (DNFB) contact sensitivity is in part mediated by suppressor thymus-derived cells (T cells) which are induced by pretreatment with the hapten 2,4-dinitrobenzenesulfonate. If lymph node cell suspensions containing suppressor cells are cultured in vitro, soluble suppressor factor (SSF) is released into the supernatant. When DNFB-immune lymph node cells are incubated with SSF, their ability to transfer contact sensitivity to normal recipients is suppressed. In order for SSF to be produced and/or released, it was necessary to paint the tolerant animals with DNFB 16 to 20 hr before the lymph node cells were cultured, suggesting that SSF was made in response to antigen stimulation. Specificity studies showed that SSF was both antigen specific and strain specific in its action. In addition, it was found that SSF could be absorbed by 2,4-dinitrophenyl-keyhold limpet hemocyanin (DNP-KLH) (not by KLH alone) and by anti-H-2 antibodies but not by trinitrophenyl-KLH, anti-immunoglobulin, or anti-DNP antibodies. Taken together, these results indicate that SSF is a product of the major histocompatibility complex which, although not antibody, has affinity and specificity for the hapten DNP. Furthermore, in order for SSF to suppress DNFB sensitivity, identity is required among genes in the H-2 complex between the donor of SSF and the immune lymph node cells.

Animals↗
PubMed1977

Soluble factors in tolerance and contact sensitivity to DNFB in mice. II. Genetic requirements for suppression of contact sensitivity by soluble suppressor factor.

Active suppression of contact sensitivity to DNFB in mice is mediated by a soluble suppressor factor (SSF) which is released in vitro by cultures of LN cells that contain antigen-specific suppressor T cells. For SSF-mediated suppression to occur, identity is required among genes in the H-2 complex between the donor of SSF and the donar of DNFB-immune LN cells. Identity in either the left half or right half of the H-2 complex was found to be both sufficient and required. Additional experiments using congeneic strains with intra-H-2 recombinants showed that the genetic homology which was required mapped to genes contained in the H-2K and/or H-2D regions of the H-2 complex.

Animals↗
PubMed1976

Tolerance and contact sensitivity to DNFB in mice. VI. Inhibition of afferent sensitivity by suppressor T cells in adoptive tolerance.

Tolerance in contact sensitivity to DNFB can be adoptively transferred to normal mice with lymph node cells from tolerant donors. This tolerance is antigen specific and is mediated by T cells, i.e., "suppressor" T cells. Experiments were carried out to investigate the mechanism(s) by which the suppressor T cells induce tolerance to DNFB contact sensitivity. The suppressor cells were effective only if they were present during the early stages of the afferent limb of sensitization. As measured by DNA synthesis, cell proliferation in the draining lymph nodes of recipients of suppressor cells was found to be significantly less than in control animals indicating that the suppressor cells acted, at least in part, by limiting or inhibiting DNFB-induced cell proliferation. This inhibition was shown to be antigen specific since the DNFB suppressor cells did not inhibit cell proliferation induced by oxazolone, an unrelated contact sensitizer. The ability to DNFB tolerant cells to block afferent sensitization pathways differs from the mechanism of tolerance to picryl chloride, reported by others, where efferent pathways are blocked.

Animals↗
PubMed1976

Anti-immunoglobulin stimulation of murine lymphocytes. I. Age dependency of the proliferative response.

The in vitro proliferative response of normal mouse spleen cells to anti-immunoglobulin (Anti-Ig) reagents was found to be an age-associated phenomenon. The response usually appears in mice when they reach 5 to 7 months of age and is rarely seen in younger animals. Anti-Ig induced proliferation was observed by using two different antisera--one polyvalent, prepared against mouse antibody-antigen complexes and one prepared against mouse IgM myeloma. Both antisera were shown to be specific for B cells by cytotoxicity and immunofluorescent staining. Glassbead separation of spleen cells showed that the anti-Ig-induced proliferation was a B cell response.

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