Cytotoxic cells induced after Chlamydia psittaci infection in mice

Lammert, Joyce K.

doi:10.1128/iai.35.3.1011-1017.1982

Cited by 33 publications

(15 citation statements)

References 28 publications

(27 reference statements)

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“…Because of the obligate intracellular lifestyle of C. trachomatis, it has been thought that CTL may also be involved in immunity to this pathogen. Past attempts to identify Chlamydia-specific CTL in vitro have been problematic (18,24,25). However, two laboratories have recently reported cytolysis of Chlamydia-infected cells by CD8 ϩ lymphocytes (3,37).…”

Section: Discussionmentioning

confidence: 99%

Gene knockout mice establish a primary protective role for major histocompatibility complex class II-restricted responses in Chlamydia trachomatis genital tract infection

1995

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Mice with disrupted ␤ 2-microglobulin (␤ 2 m ؊/؊), I-A (class II ؊/؊), or CD4 (CD4 ؊/؊) genes were examined for their capacity to resolve Chlamydia trachomatis genital tract infection. C57BL/6 and ␤ 2 m ؊/؊ mice resolved infection similarly and were culture negative by 4 to 5 weeks following infection. Conversely, major histocompatibility complex (MHC) class II ؊/؊ mice failed to resolve infection, and CD4 ؊/؊ mice showed a significant delay (2 weeks). Secondary challenge of C57BL/6, ␤ 2 m ؊/؊ , and CD4 ؊/؊ mice established that acquired protective immunity, which was characterized by an infection of shortened duration and reduced shedding of infectious organisms, developed. Serological analysis of C57BL/6 and ␤ 2 m ؊/؊ mice by enzyme-linked immunosorbent assays revealed no striking differences in the immunoglobulin subclass specificity of the anti-Chlamydia response, although some differences were observed in the magnitude of the immunoglobulin G2a (IgG2a) and IgG2b responses. Class II ؊/؊ mice produced lower-titered serum anti-Chlamydia antibodies of all isotypes. The serum antibody responses of CD4 ؊/؊ mice were similar to those of C57BL/6 mice, except that the anti-Chlamydia IgA response was delayed by approximately 3 weeks. Analysis of vaginal washes for Chlamydiareactive antibodies revealed the presence of IgG2a, IgG2b, and IgA in C57BL/6 and ␤ 2 m ؊/؊ mice and primarily of IgA in CD4 ؊/؊ mice. Vaginal washes from class II ؊/؊ mice were consistently antibody negative. Interestingly, the Chlamydia-specific IgA response in the vaginal washes of CD4 ؊/؊ mice was delayed, but its appearance coincided with decreased shedding of infectious organisms and resolution of infection. Our results demonstrate that MHC class II-restricted T-cell responses are necessary for the development of protective immunity to Chlamydia genital tract infection and that local (vaginal) anti-Chlamydia IgA antibody coincides with the resolution of infection. A substantive role for MHC class I-restricted T-cell responses in protective immunity to Chlamydia genital tract infection was not confirmed.

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Section: Discussionmentioning

confidence: 99%

Gene knockout mice establish a primary protective role for major histocompatibility complex class II-restricted responses in Chlamydia trachomatis genital tract infection

1995

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“…Although our findings strongly implicate CMI as a major factor in resolution of MoPn genital infections of mice, the exact effector mechanism remains to be determined. One such mechanism may be that of cell-mediated cytotoxicity of chlamydia-infected cells, although in vitro and in vivo data have yielded variable results (14,16,17). Others have reported that gamma interferon may be important in resolving chlamydial infections, either through macrophage activation (6,25) or by direct inhibition of intracellular replication, as has been demonstrated in various cell culture systems (7,24).…”

Section: Discussionmentioning

confidence: 99%

Resolution of chlamydial genital infection in B-cell-deficient mice and immunity to reinfection

1988

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The purpose of this investigation was to determine the relative roles of the humoral and cell-mediated immune responses in the resolution of chlamydial genital infection of mice and resistance to reinfection. To this end, female BALB/c mice were rendered B cell deficient by treatment with heterologous anti-immunoglobulin M (IgM) serum from birth. Controls were similarly treated with either normal serum or phosphate-buffered saline. Before inclusion in each experiment, aiti-IgM-treated mice were screened for the absence of IgM in serum and for the presence of cell-mediated immune responses. In addition, ppleen cells from anti-IgM-treated mice responded to concanavalin A and phytohemagglutinin but not to lipopolysaccharide. By these criteria, mice were designated B cell deficient. B-cell-deficient mice and controls were inoculated intravaginally with a suspension of mouse pnecvumonitis agent (MoPn), a Chiamydia trachomatis biovar. All B-cell-deficient mice resolved the infection. Additionally, no significant difference was seen in the course of the infection in B-cell-deficient mice when compared with controls. In contrast to control mice, B-cell-deficient mice displayed no detectable antibody responses to MoPn in serum or in genital secretions. However, both B-cell-deficient mice and controls developed delayed-type hypersensitivity and T-cell proliferative responses to MoPn. When challenged 53 days after primary infection, no significant difference was seen in the resistance of B-cell-deficient mice to reinfection when compared with that of the controls. These data indicate that cell-mediated immune mechanisms play an important role in the resolution of and resistance to chlamydial genital infection in this model.

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“…CD8 ϩ T cells comprise roughly 35% of the lymphocytes recovered from MoPn-infected genital tissue (33) and function as professional killer cells as well as a potential source of type 1 cytokines. Although early efforts to detect cell-mediated cytotoxicity against C. trachomatis-infected target cells were unsuccessful (30), cytotoxic T lymphocytes (CTL) were implicated in the detachment of Chlamydia psittaci-infected targets from culture flasks (24) and, later, in the lysis of C. psittaci (8)-or C. trachomatis (5,38,39)-infected cells. However, when the in vivo activity of CTL generated against human C. trachomatis serovars was analyzed, their capacity to protect recipients was attributed to the elaboration of IFN-␥ rather than to direct cell-mediated cytotoxicity (39).…”

mentioning

confidence: 99%

Clearance ofChlamydia trachomatisfrom the Murine Genital Mucosa Does Not Require Perforin-Mediated Cytolysis or Fas-Mediated Apoptosis

et al. 1999

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The molecular mechanisms of resistance to genital infection with the mouse pneumonitis (MoPn) strain of Chlamydia trachomatis are unknown. A role for major histocompatibility complex class II-restricted, interleukin-12-dependent CD4+T cells has been established, but the functional activity of these cells does not depend on secretion of gamma interferon. Here we examined the potential contribution of T-cell-mediated cytotoxicity and apoptosis to mucosal clearance of MoPn by using mice deficient in the molecular mediators of target cell lysis. Animals lacking perforin, Fas, Fas ligand, or both perforin and Fas ligand were infected genitally with C. trachomatis MoPn and monitored for expression of immunity to chlamydial antigens and clearance of MoPn from the genital mucosa. In each case, the profile of spleen cytokine production, the magnitude of the host antibody response, and the kinetics of chlamydial clearance were similar to those of genetically intact controls. Compensatory overproduction of tumor necrosis factor alpha, an alternate mediator of apoptosis in certain cell types, did not appear to account for the ability of mutant mice to resolveChlamydia infections. These results fail to support CD4+ T-cell-mediated apoptosis or CD8+T-cell-mediated cytotoxicity as being critical to the clearance ofC. trachomatis MoPn urogenital infections.

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Cytotoxic cells induced after Chlamydia psittaci infection in mice

Cited by 33 publications

References 28 publications

Gene knockout mice establish a primary protective role for major histocompatibility complex class II-restricted responses in Chlamydia trachomatis genital tract infection

Gene knockout mice establish a primary protective role for major histocompatibility complex class II-restricted responses in Chlamydia trachomatis genital tract infection

Resolution of chlamydial genital infection in B-cell-deficient mice and immunity to reinfection

Clearance ofChlamydia trachomatisfrom the Murine Genital Mucosa Does Not Require Perforin-Mediated Cytolysis or Fas-Mediated Apoptosis

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