Lymphocyte-Mediated Cellular Immunity in Histoplasmosis

Howard, Dexter H.; Otto, V; Gupta, Rishab K.

doi:10.1128/iai.4.5.605-610.1971

Cited by 49 publications

(35 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…9). In another study (31), nonadherent cells were required to remain with adherent macrophages for at least 3 h to mediate the inhibition of intracellular growth of Histoplasma. Since we allowed 2-3 h adherence and incubation periods in the present study, close contact of cells may have permitted specific instruction.…”

Section: Discussionmentioning

confidence: 99%

Cell-Mediated Immunity Against Besnoitia and Toxoplasma in Specifically and Cross-Immunized Hamsters and in Cultures

Hoff

Frenkel

1974

The Journal of Experimental Medicine

View full text Add to dashboard Cite

The capacity of hamster peritoneal cell populations to control viability and growth of Besnoitia and Toxoplasma organisms was assessed in vivo and in vitro. Immunized hamsters reduced the homologous organisms 100- to 10,000-fold over a 5-day period, but the heterologous infection increased 100- to 1,000-fold in numbers, similar as in the nonimmune controls. Passively administered antibody was ineffective although lytic cofactors were supplied by hamsters. In cultures, peritoneal cells from Besnoitia-immune hamsters delayed the growth of homologous parasites to an average of 38.5 h per division; however, in Toxoplasma-immune and nonimmune cells, Besnoitia divided every 12.8 h. Specificity of immunity was pronounced against both infections. With cross-infections, Toxoplasma-immune cultures did not effectively delay Besnoitia growth; however, Besnoitia-immune cultures reduced Toxoplasma growth by one-half. Co-cultivation experiments demonstrated that specifically committed lymphocytes could instruct macrophages to reduce the homologous organism 10-fold, whereas heterologous organisms were reduced only 2-fold. Lymphocyte supernatants initiated hypersensitivity as indicated by macrophage activation and giant cell formation in culture. However, these supernatants did not transfer infection immunity. Lymphokines could account for the hypersensitivity phenomena, but cell-mediated infection immunity in this model required close lymphocyte-macrophage proximity. These studies indicate that a number of distinct processes including delayed hypersensitivity, macrophage activation, and specific cellular immunity are acting simultaneously during latent Besnoitia infection of hamsters. All three processes are mediated by lymphoid cells and appear to be specifically induced. Although activated macrophages develop some heightened nonspecific capabilities, these were several orders of magnitude below the specific effects.

show abstract

Section: Discussionmentioning

confidence: 99%

Cell-Mediated Immunity Against Besnoitia and Toxoplasma in Specifically and Cross-Immunized Hamsters and in Cultures

Hoff

Frenkel

1974

The Journal of Experimental Medicine

View full text Add to dashboard Cite

show abstract

“…DISCUSSION It has been established in experimental histoplasmosis that T cells from an immune animal transfer immunity against lethal challenge to a naive recipient and that such cells activate normal macrophages via soluble factor(s) (19,41). One of the macrophage-activating factors that has been characterized is IFN-y (41,42).…”

Section: Resultsmentioning

confidence: 99%

Toxicity and Immunogenicity of Neisseria meningitidis Lipopolysaccharide Incorporated into Liposomes

1992

Infect Immun

View full text Add to dashboard Cite

“…Histoplasma capsulatum is a facultative intracellular parasite of the macrophages of animals. Acquired immunity to infection by this fungus is mediated by immune lymphocytes (8). Recombinant murine gamma interferon (rMuIFN--y), as well as lymphokines prepared from immune splenocytes or concanavalin A-stimulated T-cell hybridomas, activates normal macrophages to inhibit the intracellular growth of H. capsulatum (11)(12)(13).…”

mentioning

confidence: 99%

Macrophage cell lines P388D1 and IC-21 stimulated with gamma interferon fail to inhibit the intracellular growth of Histoplasma capsulatum

Wu-Hsieh

Howard

1989

Infect Immun

View full text Add to dashboard Cite

Histoplasma capsulatum, a facultative intracellular parasite of macrophages, grows within mononuclear cells of the P388D1 and IC-21 cell lines with a generation time comparable to that with which it grows in normal resident peritoneal macrophages (10 +/- 2 h). Recombinant murine gamma interferon (rMuIFN-gamma) activates P388D1 cells to express la antigens but not to inhibit the intracellular growth of H. capsulatum, alone or in combination with lipopolysaccharide. IC-21 cells also could not be activated to fungistasis with rMuIFN-gamma. Explanted resident peritoneal macrophages of the C57BL/6 (from which the IC-21 cell line derives), C3H/HeJ, DBA/2 (from which the P388D1 cell line derives), A/J, and SJL/J strains of mice were all stimulated by rMuIFN-gamma to inhibit the fungus.

show abstract

Lymphocyte-Mediated Cellular Immunity in Histoplasmosis

Cited by 49 publications

References 10 publications

Cell-Mediated Immunity Against Besnoitia and Toxoplasma in Specifically and Cross-Immunized Hamsters and in Cultures

Cell-Mediated Immunity Against Besnoitia and Toxoplasma in Specifically and Cross-Immunized Hamsters and in Cultures

Toxicity and Immunogenicity of Neisseria meningitidis Lipopolysaccharide Incorporated into Liposomes

Macrophage cell lines P388D1 and IC-21 stimulated with gamma interferon fail to inhibit the intracellular growth of Histoplasma capsulatum

Contact Info

Product

Resources

About