Experimental murine candidiasis: cell-mediated immunity after cutaneous challenge. 1980

S A Moser, and J E Domer, and F J Mather

Male CBA/J mice, sensitized by cutaneous inoculation with viable Candida albicans blastospores, were used to study in vivo and in vitro cellular immune responses. Three antigens of C. albicans, viz., a cell wall glycoprotein (GP), a membrane extract (ppt-HEX), and soluble cytoplasmic substances (SCS), were used in vitro in a lymphocyte stimulation assay, whereas the GP and ppt-HEX were used in vivo to detect delayed hypersensitivity by the footpad assay. Delayed hypersensitivity to GP and ppt-HEX was transferred from sensitized donors to naive recipients with peritoneal exudate cells and not with serum. Moreover, the transfer of the reactivity to ppt-HEX was abrogated by the prior treatment of the transfer suspension with anti-theta 1.2 serum and complement. The in vitro lymphocyte response to GP and ppt-HEX correlated qualitatively with the in vivo responses. SCS, a preparation shown to be ineffective in vivo previously, did stimulate lymphocytes from sensitized animals in vitro. The in vitro response to Candida antigens, as well as phytohemagglutinin, was abolished by treatment of the lymphocyte suspension with anti-thymocyte 1.2 serum before assay, whereas anti-immunoglobulin serum had less effect on these responses. The in vivo and in vitro reactivity to the Candida antigens, therefore, was dependent upon viable T-lymphocytes. Preliminary specificity studies were carried out in the lymphocyte stimulation assay, using lymphocytes from mice infected with C. albicans tested against ppt-HEX preparations extracted from two other species of Candida, C. tropicalis and C. guillermondii, and from two other pathogenic yeast forms, Histoplasma capsulatum and Blastomyces dermatitidis. Significant cross-reactivity was observed with C. tropicalis only, a species which is known to be serologically related to C. albicans.

UI MeSH Term Description Entries
D006968 Hypersensitivity, Delayed An increased reactivity to specific antigens mediated not by antibodies but by sensitized T CELLS. Hypersensitivity, Tuberculin-Type,Hypersensitivity, Type IV,Tuberculin-Type Hypersensitivity,Type IV Hypersensitivity,Delayed Hypersensitivity,Delayed Hypersensitivities,Hypersensitivity, Tuberculin Type,Tuberculin Type Hypersensitivity,Tuberculin-Type Hypersensitivities,Type IV Hypersensitivities
D007111 Immunity, Cellular Manifestations of the immune response which are mediated by antigen-sensitized T-lymphocytes via lymphokines or direct cytotoxicity. This takes place in the absence of circulating antibody or where antibody plays a subordinate role. Cell-Mediated Immunity,Cellular Immune Response,Cell Mediated Immunity,Cell-Mediated Immunities,Cellular Immune Responses,Cellular Immunities,Cellular Immunity,Immune Response, Cellular,Immune Responses, Cellular,Immunities, Cell-Mediated,Immunities, Cellular,Immunity, Cell-Mediated,Response, Cellular Immune
D008198 Lymph Nodes They are oval or bean shaped bodies (1 - 30 mm in diameter) located along the lymphatic system. Lymph Node,Node, Lymph,Nodes, Lymph
D008213 Lymphocyte Activation Morphologic alteration of small B LYMPHOCYTES or T LYMPHOCYTES in culture into large blast-like cells able to synthesize DNA and RNA and to divide mitotically. It is induced by INTERLEUKINS; MITOGENS such as PHYTOHEMAGGLUTININS, and by specific ANTIGENS. It may also occur in vivo as in GRAFT REJECTION. Blast Transformation,Blastogenesis,Lymphoblast Transformation,Lymphocyte Stimulation,Lymphocyte Transformation,Transformation, Blast,Transformation, Lymphoblast,Transformation, Lymphocyte,Activation, Lymphocyte,Stimulation, Lymphocyte
D008297 Male Males
D008808 Mice, Inbred CBA An inbred strain of mouse that is widely used in BIOMEDICAL RESEARCH. Mice, CBA,Mouse, CBA,Mouse, Inbred CBA,CBA Mice,CBA Mice, Inbred,CBA Mouse,CBA Mouse, Inbred,Inbred CBA Mice,Inbred CBA Mouse
D002176 Candida albicans A unicellular budding fungus which is the principal pathogenic species causing CANDIDIASIS (moniliasis). Candida albicans var. stellatoidea,Candida stellatoidea,Dematium albicans,Monilia albicans,Myceloblastanon albicans,Mycotorula albicans,Parasaccharomyces albicans,Procandida albicans,Procandida stellatoidea,Saccharomyces albicans,Syringospora albicans
D002177 Candidiasis Infection with a fungus of the genus CANDIDA. It is usually a superficial infection of the moist areas of the body and is generally caused by CANDIDA ALBICANS. (Dorland, 27th ed) Candida Infection,Moniliasis,Candida Infections,Candidiases,Infection, Candida,Moniliases
D003165 Complement System Proteins Serum glycoproteins participating in the host defense mechanism of COMPLEMENT ACTIVATION that creates the COMPLEMENT MEMBRANE ATTACK COMPLEX. Included are glycoproteins in the various pathways of complement activation (CLASSICAL COMPLEMENT PATHWAY; ALTERNATIVE COMPLEMENT PATHWAY; and LECTIN COMPLEMENT PATHWAY). Complement Proteins,Complement,Complement Protein,Hemolytic Complement,Complement, Hemolytic,Protein, Complement,Proteins, Complement,Proteins, Complement System
D000818 Animals Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA. Animal,Metazoa,Animalia

Related Publications

S A Moser, and J E Domer, and F J Mather
October 1986, Parasitology today (Personal ed.),
S A Moser, and J E Domer, and F J Mather
January 1985, Annales de l'Institut Pasteur. Immunologie,
S A Moser, and J E Domer, and F J Mather
May 1993, Infection and immunity,
S A Moser, and J E Domer, and F J Mather
March 1994, Infection and immunity,
S A Moser, and J E Domer, and F J Mather
June 1994, Trends in microbiology,
S A Moser, and J E Domer, and F J Mather
October 1976, Journal of the Reticuloendothelial Society,
S A Moser, and J E Domer, and F J Mather
May 1988, The British journal of dermatology,
S A Moser, and J E Domer, and F J Mather
February 1986, Human pathology,
S A Moser, and J E Domer, and F J Mather
May 1981, The Indian journal of medical research,
S A Moser, and J E Domer, and F J Mather
November 1978, The Journal of infectious diseases,
Copied contents to your clipboard!