Delayed-type Hypersensitivity Skin Reactions Research Articles

Effect of Infectious Bursal Disease Virus on the Immunological Responsiveness of the Chicken

The immunological response of chickens infected at 28 days of age with infectious bursal disease virus (IBDV) was examined. Cellular immunity was studied by the graft-versus-host reaction and delayed type hypersensitivity skin reactions to tuberculin. Antibody responses to sheep red blood cells (S-RBC’s) were tested by a direct hemagglutination test. Circulating levels of immunoglobulins (Ig’s) IgM, IgG and IgA were monitored by the radial immunodiffusion test. The results of the graft-versus-host reaction and delayed type hypersensitivity reactions were similar for both the infected and control chicks. IBDV significantly reduced the primary antibody response to S-RBC’s, but had no marked effect on the secondary antibody response. Chicks infected with IBDV had normal levels of serum IgM and IgG, but significantly lower levels of IgA when compared to uninfected control birds.

Cells involved in cell-mediated and transplantation immunity in the rabbit. VI. The dissociation between cell-mediated and humoral immunity to particulate antigens.

It was demonstrated that, in the rabbit, there is a distinct dissociation between the cells activated in the induction of the humoral and delayed hypersensitivity states of immunity. This was best proved by the fact that 800 rad whole body irradiation, which results in death or inactivation of the antigen-reactive cells involved in humoral immunity, did not abrogate the capacity of the rabbit to be sensitized to give delayed-type hypersensitivity skin reactions. It is concluded that these two types of immunity result from the activation of two different cell pathways.

Location of the antigen, antibody and antigen-antibody complexes in delayed-type hypersensitivity skin reactions to horseradish peroxidase.

The sites of intradermally injected horseradish peroxidase (HRP), of its antibody and of HRP-anti-HRP antibody complexes were investigated in the dermis of rabbits showing strong skin reactions of delayed hypersensitivity against HRP. Comparison was made with the location of intradermally injected HRP and its antibody in the dermis of immunized rabbits showing slight degrees of hypersensitivity of a nondelayed type and with the location of intradermally injected HRP in the dermis of nonimmunized animals. In all skin reactions of delayed hypersensitivity, a considerable proportion of the injected antigen was associated with collagen fibers, the reaction product appearing as "dots," "rodlets" and "strands" in linear array on individual collagen fibers in the interior of the bundles or as strands coating the outermost surface of the bundles. The reaction for the antibody was positive at the same sites. It was suggested that receptors for antigen-antibody complexes may be associated with collagen fibers. Free granular deposits containing antigen-antibody complexes seemed to originate from the collagen-associated granules after their enlargement and release. The extracellular granules often adhered to the antibody-positive surface membranes of lymphocytes. Other granular deposits (antigen-antibody complexes) seemed to be phagocytosed by monocytes (macrophages) and fibroblasts. In areas of tissue injury in the upper dermis, many mononuclear cells showed the reaction for the antibody on their cell surface. Aggregations of such cells were often located close to disintegrating bundles of collagen fibers. It was suggested that the encounter of the antigen and the antibody (antigen-antibody complexes) on the surfaces of cells and of collagen may trigger the release of cytotoxic factors. A few lymphocytes in the dermis of hypersensitive rabbits contained the specific antibody on their cell surface before skin lesions were elicited.