Important note: Information in this article was accurate in 1999. The state of the art may have changed since the publication date.
Role of NK cells in early host response to chlamydial genital infection.
Infect Immun. 1998 Dec;66(12):5867-75. Unique Identifier : AIDSLINE MED/99043917 Tseng CT; Rank RG; Department of Microbiology and Immunology, University of Arkansas; for Medical Sciences, Little Rock, Arkansas 72205, USA.
Abstract:
The cell-mediated immune response has been documented to be the major protective immune mechanism in mice infected genitally with the agent of mouse pneumonitis (MoPn), a biovar of Chlamydia trachomatis. Moreover, there is strong evidence to indicate that gamma interferon (IFN-gamma) is a major effector mechanism of the cell-mediated immune response. Previous studies from this laboratory have also reported that the dominant cell population in the genital tract is the CD4 Th1 population. When experiments were performed by the enzyme-linked immunospot assay, high numbers of cells producing IFN-gamma were found in the genital tract, concomitant with resolution of the infection; however, in addition, an increase in IFN-gamma-producing cells which were CD4(-) was seen early in the infection. Since natural killer (NK) cells produce IFN-gamma and have been found to participate in the early responses in other infections, we hypothesized that NK cells are responsible for early IFN-gamma production in the murine chlamydial model. NK cells were quantified by the standard YAC-1 cytotoxicity assay and were found to appear in the genital tract as early as 12 h after intravaginal infection with MoPn. The cells were confirmed to be NK cells by abrogation of YAC-1 cell cytotoxicity by treatment in vitro and in vivo with anti-asialo-GM1. The early IFN-gamma response could also be depleted by treatment with anti-asialo-GM1, indicating that NK cells were responsible for the production of this cytokine. Of interest was our observation that depletion of NK cells also exacerbated the course of infection in the mice and elicited a Th2 response, as indicated by a marked increase in immunoglobulin G1 antibody. Thus, these data demonstrate that NK cells are not only responsible for the production of IFN-gamma early in the course of chlamydial genital tract infection but are also, via IFN-gamma, a significant factor in the development of the Th1 CD4 response and in the control of the infection.
Keywords: JOURNAL ARTICLE Animal Chlamydia trachomatis/*IMMUNOLOGY Chlamydia Infections/*IMMUNOLOGY Cytokines/ANALYSIS Female G(M1) Ganglioside/ANALYSIS Genitalia, Female/IMMUNOLOGY IgG/ANALYSIS Ilium Immunoglobulin Isotypes/ANALYSIS Interferon Type II/BIOSYNTHESIS Killer Cells, Natural/*IMMUNOLOGY Lymph Nodes/IMMUNOLOGY Lymphocyte Depletion Mice Mice, Inbred BALB C Pneumonia/MICROBIOLOGY Rodent Diseases/MICROBIOLOGY Support, U.S. Gov't, P.H.S. Th1 Cells/IMMUNOLOGY Vaginal Diseases/*IMMUNOLOGY 990330
A9931064
AEGiS presents published material, reprinted with permission and neither endorses nor opposes any material. All information contained on this website, including information relating to health conditions, products, and treatments, is for informational purposes only. It is often presented in summary or aggregate form. It is not meant to be a substitute for the advice provided by your own physician or other medical professionals. Always discuss treatment options with a doctor who specializes in treating HIV.
Important note: Information in this article was accurate in 1999. The state of the art may have changed since the publication date.
