Nonspecific and Candida-Specific Immune Responses in Mice Suppressed by Chronic Administration of Anti-μ

Abstract

CBA/J mice were immunosuppressed by repeated administration of goat antibody specific for mu chain of immunoglobulin M (IgM) and tested for nonspecific and Candida albicans-specific immune responses. Immunosuppression was demonstrated by a dramatic reduction in the number of antibody-forming cells in the spleens of anti-mu-treated mice when immunized with sheep erythrocytes, by greatly reduced in vitro responsiveness of both spleen and lymph node lymphocytes from anti-mu-treated mice to lipopolysaccharide, and by a large reduction in the number of splenic IgM-positive cells. T cell function, on the other hand, appeared to be relatively unaltered in anti-mu-treated animals, in the cytotoxic T lymphocyte activity against an allogeneic target was similar in splenocyte cultures from anti-mu- and mock-treated animals, and splenic and lymph node lymphocytes proliferated in response to concanavalin A in a lymphocyte stimulation assay. Moreover, Candida-specific delayed hypersensitivity to two different Candida antigens, one cell wall-derived (GP) and the other cell membrane-derived (BEX), was of comparable intensity in immunosuppressed and normal animals. When anti-mu- and mock-treated mice were immunized by the cutaneous inoculation of viable C. albicans blastospores and then challenged intravenously to assess the development of protective immunity, only mock-treated animals, male and female, had significant (p less than or equal to 0.05) protective responses demonstrable by reduction in the number of colony-forming units cultured from their kidneys 28 days after intravenous challenge. If consideration was given to the number of animals which had cleared Candida completely from the kidney, however, there appeared to be protective responses operative in the female anti-mu-treated animals as well. Neither anti-mu-treated males nor females, when immunized and challenged with C. albicans, produced Candida-specific antibody detectable by counterimmunoelectrophoresis, whereas all immunized and challenged mock-treated animals produced antibody. The data are consistent with the hypothesis that anti-mu treatment has little effect on multiple cellular immune functions, including those specific for C. albicans, and the combination of antibody, cell-mediated immunity and innate defenses are responsible for solid systemic defense against the fungus.

Anti-enolase antibodies partially protective against systemic candidiasis in mice

“…It is likely that antibody‐dependent antigen presentation to T‐cells is involved, allowing earlier recognition of C. albicans cells, probably combined with enhancement of cell‐mediated mechanisms, which might have resulted in increased survival. Therefore we conclude, as have others, that protective immunity against systemic candidiasis involves a combination of innate defenses, and humoral and cellular immunity [28].…”

Vaccination with Recombinant N-Terminal Domain of Als1p Improves Survival during Murine Disseminated Candidiasis by Enhancing Cell-Mediated, Not Humoral, Immunity

“…Although we and others (28,64) have found that B-celldeficient mice are not more susceptible to candidemia than wild-type controls are, numerous studies have reported that passive immunization against C. albicans improves survival during murine disseminated candidiasis (18,20,45,60). Indeed, a monoclonal antibody directed against a C. albicans heat shock protein (35) is currently in clinical trials.…”

A cell surface/plasma membrane antigen of Candida albicans

“…These layers are intimately involved in the shape of the cell, antigenicity and secretion of hydrolytic enzymes. The cell wall of C. albicans has thus been a major area of investigation on candidal-host interactions mainly because of the role in adherence to its host (Levitz et al, 1987;Calderone et al, 1984;Maisch & Calderone, 198 l), and interactions with host immune systems (Calderone et al, 1988;Kuruganti et al, 1988). The plasma membrane, on the other hand, is of particular importance in homoeostatic control and susceptibility to antifungal agents (Shepherd, 1987).…”