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Alloxan diabetic mice do not easily develop anaphylactic shock, and formation of IgE antibodies to sensitizing antigen almost ceases in these animals. Also, mice sensitized as normoglycaemic and then made diabetic are to a great degree protected from anaphylaxis. although they form minute but measurable amounts of IgE antibodies. Immune cells transferred into diabetic mice lose their ability to form IgE, while cells from immune diabetic mice, which in the hypoinsulinaemic milieu of donors do not synthesize appreciable amounts of IgE, regain this ability upon transfer into normal recipients. We conclude that the IgE response is very insulin-dependent and that insulin deficiency affects IgE-forming cells directly or indirectly via its influence on T helper cells. In the current study we also considered whether hyperglycaemia may influence the effector stage of anaphylactic reactions. To test this, massive doses of glucose were given to normoglycaemic mice, which increased their blood glucose level to that seen in diabetic mice and prevented local anaphylactic reactions when these mice were injected with monoclonal IgE antibody and challenged locally with antigen. [ABSTRACT FROM AUTHOR]

Alloxan diabetic BALB/c mice with high hyperglycaemia levels (⩾ 600 mg/100 ml) when immunized either with T-dependent (SRBC) or T-independent (TNP-LPS) antigens show a significant decrease in the number of specific PFC when compared with normo-glycaemic controls. Moderate diabetes (> 350 mg/100 ml) does not affect the immune response and in some experiments a slight increase of anti-SRBC plaques was seen. In transfer experiments primed spleen cells of either diabetic or normal donors gave much better responses when transferred to normal rather than diabetic X-irradiated recipients. In Mishell-Dutton (MD) cultures the anti-SRBC response of CBA spleen cells was moderately reduced only when the blood glucose level of cell donors exceeded 500 mg/100 ml. Glucose added to MD cultures of normal spleen cells diminished significantly the number of SFC when in concentrations exceeding 600 mg/100 ml. The data indicate that in diabetic animals B-lymphocyte function may be affected but give no clear-cut answer to whether this is also true for T-helper cells. Disabled lymphocytes, whatever population they represent, may partially recover when transferred into normo-insulinic milieu. It may be inferred that under conditions tested neither hyperglycaemia nor excess of corticosteroid accounted significantly for the impaired humoral responses in diabetic animals. These experiments imply, however, that in hypoinsulinaemia the lack of saturation of insulin receptors on the lymphocyte, and possibly also macrophage, membranes renders these cells functionally inactive presumably due to accumulation of cyclic AMP in the cell membrane. [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]

It has been shown that CBA mouse lymphocytes cultured in the presence of allogeneic fibroblasts or syngeneic polyoma virus-induced tumour cells became specifically immunized. These immunized lymphocytes, however, are by themselves non-cytotoxic and only cause target cell killing when mixed with normal macrophages. The reaction is immunologically specific and seems to depend on the antigenic differences between lymphocytes and target cells. The mechanism of the interaction between the immunized lymphocytes and the normal macrophages in the cytotoxic killing of target cells is discussed. [ABSTRACT FROM AUTHOR]

Gastrectomy in mice affects the cell-mediated (CMI) and humoral immunity in a diverse fashion, such as CMI (contact sensitivity reaction) is severely impaired and antibody response is enhanced. Both effects are transient and disappear several days after surgery. While suppression of contact sensitivity is mediated by non-specific Ly 1-2+, L-J+ suppressor T cells generated by surgical stress, the mechanisms of enhancement of antibody response is unknown. We assume that the split unresponsiveness induced by surgical trauma has a clear survival advantage. Increased antibody production is the major defence mechanism against bacterial infections, while decrease of CMI prevents autoimmune response against altered (damaged) self structures. [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]