I-E/I-C region-associated induction of murine gamma interferon by a haplotype-restricted polyclonal T-cell mitogen derived from Mycoplasma arthritidis

Cole, Barry C.; Thorpe, R N

doi:10.1128/iai.43.1.302-307.1984

Cited by 16 publications

(6 citation statements)

References 23 publications

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“…Mice possessing the H-2k or H-2d haplotype were susceptible, whereas those expressing H-2b appeared to be more resistant (10). Further influences asserted by the MHC haplotype were on an ulcerative dermal coagulation necrosis upon subcutaneous injection of M. arthritidis (7) and a reactivity of mouse lymphocytes toward M. arthritidis supernatants (MAS) acting as a soluble T-cell mitogen (5,9). Spleen cells from several inbred rat strains also showed a differential response towards MAS, but this was not associated with the rat MHC, RTJ (6).…”

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confidence: 99%

Strain differences in sensitivity of rats to Mycoplasma arthritidis ISR 1 infection are under multiple gene control

et al. 1990

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At least 5 female rats from each of 24 inbred (ACI, AS, BDIX, BH, BN, BS, BUF, DA, LE, LEW, MWF, OM, SPRD-Cu3, W-Krypt, and WKY), RTI congenic [BH.lL(LEW), LEW.lA(AVN), LEW.lC(WIST), LEW.lLV3(BH), LEW.lK(SHR), and LEW.1N(BN)], and F1 hybrid [(LEW x BN)F1, (LEW.1W x LEW.1A)F1, and (LEW x LEW.1W)F1] strains, representing eight independent major histocompatibility complex (MHC) haplotypes (a, b, c, dvl, k, 1, n, and u) and five related RTI haplotypes (avi, lvl, 1v3, uv2, and uv3), were inoculated intravenously with Mycoplasma arthritidis, and the severity of the polyarthritis that developed was determined by estimating arthritis scores and weight reductions. The 24 inbred, congenic, and F1 hybrid rat strains differed considerably in their sensitivity to infection with M. arthritidis and in the severity of the polyarthritis that they developed. Statistical evaluation showed that in the acute phase (days 1 to 42 after infection) as well as in the chronic phase (days 39 to 121 after infection) of the disease, the means of the arthritis scores for the strains form a continuous variation without significant interruptions, with the very sensitive LEW rats, the RTI congenic rats on LEW background, the F1 hybrids with LEW, and the MWF, BS, BH, and DA rats on one end and the resistant WKY, BUF, W-Krypt, LE, and OM rats on the other end. A continuous variation was also observed for the means of the growth rates. There were, however, no significant differences between the sensitive and the resistant rat strains in the antibody titers determined by complement fixation test and enzyme immunoassay. Heritabilities of arthritis scores were calculated for all strains (h2 = 0.39 to 0.62), for the RTI congenic strains (h2 = 0.04 to 0.14), and for several strains with identical MHC genes (h2 = 0.61 to 0.93). The results show that non-MHC genes are probably responsible for the sensitivity of rats to infection with M. arthritidis.Animals. Up to 5 female rats from each of 24 inbred (ACI/

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confidence: 99%

Strain differences in sensitivity of rats to Mycoplasma arthritidis ISR 1 infection are under multiple gene control

et al. 1990

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“…tested (Table III). The interferons induced by the three mitogens were acid-labile, and we assume them to represent IFN-y, since in mouse spleen cells the same mitogen induced IFN-y [5]. Definitive proof, however, is lacking in our rat experiments, since antisera to rat IFN-y were not available.…”

Section: Resultsmentioning

confidence: 91%

“…MAS, besides inducing a lymphoproliferative response, recently has also been found to induce IFN-y in mouse spleen cell cultures [5], and we were interested in testing whether this was also true of rat spleen cells. MAS was indeed as potent as PHA or Con A in inducing IFN.…”

Section: Discussionmentioning

confidence: 99%

Lymphoproliferative Responses of Spleen Cells of Inbred Rat Strains to Mycoplasma arthritidis Mitogen

et al. 1984

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A potent mitogen for T lymphocytes of various species has recently been isolated from the supernatant of cultured Mycoplasma arthritidis organisms (MAS). In the mouse, reactivity to this mitogen has been observed to be controlled by the I-E subregion of the major histocompatibility complex. We have analysed the responses of spleen cells from several inbred rat strains covering practically all known haplotypes of the major histocompatibility complex of the rat (RT1). Unlike in the mouse, all of these responded well to MAS, except for the BN rat strain, which is a low responder to all T-cell mitogens, including phytohaemagglutinin and concanavalin A. This unresponsiveness, however, appeared to be unrelated to the RT1 haplotype, since LEW.1N rats carrying the same RT1n haplotype as BN animals responded well. Mice of the strain C57BL/6 are non-responders to MAS, but--as previously shown--their spleen cell responses can be reconstituted by the addition of 2-mercaptoethanol. No such reconstitution was observed for the low responsiveness of BN rat spleen cells. Stimulation with MAS induced high titres of interferon (presumably gamma interferon) in spleen cells from all rat strains tested. Spleen cells from BN rats produced lower interferon activities than those from other strains.

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“…This finding may be relevant in the context of immunopathology. Recent experiments have indicated that MAS is also capable of inducing gamma interferon production by T lymphocytes [7], a phenomenon that is being investigated further in our laboratory.…”

Section: Discussionmentioning

confidence: 91%

Lymphoproliferation Induced in Mouse Spleen Cells by Mycoplasma arthritidis Mitogen

et al. 1984

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Spleen cells of various mouse strains (e.g. BALB/c, C311, and CBA) reacted towards MAS (a mitogen derived from supernatants of cultured Mycoplasma arthritidis) with a marked lymphoproliferative response. This reactivity was T-cell-dependent. It was reduced by 90% after removal of macrophages by passage of the spleen cells through Sephadex G-10 columns. Addition of 2-mercaptoethanol (2-ME) to macrophage-depleted CBA spleen cells completely restored the response to MAS. Spleen cells of C57BL/6 and C57BL/10 mice were unreactive to MAS, even in the presence of macrophages, and this non-reactivity was controlled by the I-region of H-2. Other mouse strains that, similarly to C57BL/6, lack the expression of I-E on the cell surface (that is, mice of the haplotype H-2f, H-2q, and H-2s) were also non-responsive to MAS. However, the addition of 2-ME to spleen cells of non-responder mice resulted in high lymphoproliferative responses to MAS, which were as high as those of CBA spleen cells. The reaction of C57BL/6 spleen cells to MAS in the presence of 2-ME again was T-cell-dependent, as shown by data with spleen cells of homozygous nude mice and spleen cells treated by anti-thy-1 and C. A macrophage dependency of this response was also evident. When C57BL/6 spleen cells were vigorously freed of accessory cells by the use of nylon wool columns, the MAS response could no longer be restored by 2-ME.

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I-E/I-C region-associated induction of murine gamma interferon by a haplotype-restricted polyclonal T-cell mitogen derived from Mycoplasma arthritidis

Cited by 16 publications

References 23 publications

Strain differences in sensitivity of rats to Mycoplasma arthritidis ISR 1 infection are under multiple gene control

Strain differences in sensitivity of rats to Mycoplasma arthritidis ISR 1 infection are under multiple gene control

Lymphoproliferative Responses of Spleen Cells of Inbred Rat Strains to Mycoplasma arthritidis Mitogen

Lymphoproliferation Induced in Mouse Spleen Cells by Mycoplasma arthritidis Mitogen

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