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C3H/HeN mice were immunized to induce contrasuppressor T-cell (Tcs) activity, splenic T cells from these mice were fused with the BW5147 thymoma, and the resulting hybridomas were tested for their ability to produce a contrasuppressor T-cell factor (TcsF). Nine TcsF-producing hybridomas were preliminarily identified by their ability to inhibit the effect of antigen-specific suppressor T-cell factor (TsF) on the adoptive transfer of contact sensitivity. One of these hybrids, AF5.C6, was cloned, the production of a contrasuppressor factor confirmed, and the high-titred TcsF produced by this cloned hybrid characterized. Hybridoma-derived TcsF is antigen-specific and specifically binds its antigen, but does not bear immunoglobulin (Ig) determinants. Thus, hybridoma-derived TcsF is serologically and functionally identical to an antigen-specific contrasuppressor factor for contact sensitivity, whose production from splenocyte cell cultures has previously been described. The generation of a hybridoma secreting a contrasuppressor factor identical to that produced by spleen cells significantly strengthens the hypothesis that the phenomenon of T-cell contrasuppression is mediated by a specific subset of cells whose activity is contrasuppressive. The further advantages of employing T-cell hybridomas for functional, biochemical and molecular genetic analyses of contrasuppression are also discussed. [ABSTRACT FROM AUTHOR]

Alloxan-diabetic mice of Swiss, CBA and DBA/2 strains show a significant depression of contact sensitivity to oxazolone, as compared with normoglycaemic control animals, which is accompanied by the involution of the thymus and spleen. Insulin treatment partially restores the contact sensitivity in diabetic animals and also increases the weight of lymphatic organs. In contrast, the non-specific inflammatory response to oxazolone is not impaired in insulin-deficient mice. Further experiments have shown that neither sensitized lymphocytes of control animals given to diabetic mice, nor sensitized lymphocytes of diabetic mice injected into normoglycaemic recipients, were able to transfer passively any significant contact sensitivity. It is suggested that in alloxan-diabetic mice the function of T lymphocytes is affected. [ABSTRACT FROM AUTHOR]

Mice sensitized to oxazolone show contact sensitivity which can be assessed by painting oxazolone on the ear and measuring the increase in ear thickness at 24 hours. Contact sensitivity can be transferred passively by peritoneal exudate, lymph node and bone marrow cells. When CBA mice are challenged immediately after transfer, at a 3:1 donor recipient ratio, the peritoneal exudate cells give bigger transferred reactions than lymph node cells. The converse is true on challenge at 6 days after transfer, at which time the lymph node cells give bigger transferred reactions than the peritoneal exudate cells. These results suggest that different types or functional states of cells are involved in these two types of transfer. The possibility that the successful transfer with delayed challenge by lymph node cells was due to active sensitization by antigen transferred with the cells, was made unlikely by passive transfer into ‘tolerant’ recipients. Mice first show contact sensitivity when challenged at 3 days (about 72 hours) after sensitization. The lymph nodes develop the ability to transfer contact sensitivity with delayed challenge at the same time but the bone marrow only acquires this activity at 5 days. [ABSTRACT FROM AUTHOR]

Mice infected with Mycobacteriurn lepraemurium showed marked histological changes in the thymus and lymph nodes. In the thymus there was a progressive depletion of lymphoid cells and replacement by macrophages, many of which contained bacilli in the advanced stages of the disease. In lymph nodes there was depletion. of paracortical immunoblasts and accumulation of macrophages. Infected mice showed impaired cell-mediated immune responses, including delayed rejection of skin grafts and depression or absence of contact sensitivity. Humoral immune responses to bovine serum albumin and sheep erythrocytes in infected mice were normal. The defect in cell-mediated immune responses is thought to be secondary to the massive infection, and is discussed in relation to impaired immune responses in human lepromatous leprosy. [ABSTRACT FROM AUTHOR]