Publications
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Müller I, Kropf P, Etges RJ, et al., 1993, Gamma interferon response in secondary Leishmania major infection: role of CD8+ T cells., Infect Immun, Vol: 61, Pages: 3730-3738, ISSN: 0019-9567
CD8+ T cells have been shown to contribute to the rapid resolution of secondary lesions developing in immune mice challenged with Leishmania major. In the present study, we assessed directly the participation of specific CD8+ T cells in the memory response induced in immune mice by reinfection. Lymphocyte populations from reinfected immune mice exhibit marked secondary gamma interferon (IFN-gamma) responses. The participation of IFN-gamma-producing CD8+ T cells in the memory response elicited by secondary infectious challenge was demonstrated in both genetically resistant immune CBA mice and genetically susceptible immune BALB/c mice that were rendered resistant by administration of anti-CD4 monoclonal antibody in the early phase of the primary infection. The protective function of CD8+ T cells in experimental murine cutaneous leishmaniasis might thus be explained in part by their ability to secrete IFN-gamma. In this context, the neutralization of IFN-gamma at the time of reinfection reduced the Leishmania-specific delayed-type hypersensitivity response, showing that this cytokine is involved in the recall of immunological memory to L. major in vivo.
Stefani MM, Müller I, Louis J, 1993, Leishmania major infection in BALB/c mice: protection or exacerbation by treatment with different doses of BCG., Res Immunol, Vol: 144, Pages: 233-243, ISSN: 0923-2494
The effect of live bacillus Calmette-Guérin (BCG), administered intraperitoneally to BALB/c mice, upon the development of lesions induced by subcutaneous infection with Leishmania major was examined. Lesions in mice given 10(7) BCG colony-forming units (CFU) 9 days before challenge with L. major were less severe and contained significantly fewer parasites than those of similarly infected control mice not given BCG. This effect of treatment with high doses of BCG upon the development of leishmanial lesions was observed using L. major promastigotes and amastigotes, whether or not 10(6) live BCG was included in the parasite inoculum. Lesions in mice given 5 x 10(4) BCG CFU 14 days before infection with L. major contained significantly fewer parasites than those of control mice not given BCG. Mice treated with low doses of BCG and infected with an L. major inoculum also comprising BCG exhibited larger lesions that contained more parasites. Interestingly, compared to naive mice infected with L. major, infection of naive mice with L. major mixed with live BCG consistently led to the development of more severe lesions that contained higher numbers of parasites. No correlation was found between the effect of BCG on the development of lesions induced by L. major and the amounts of IFN gamma, IL5 and TNF produced after in vitro antigenic challenge of either draining lymph node or spleen cells, the antigenic challenge being either live BCG or live L. major.
Rossi-Bergmann B, Müller I, Godinho EB, 1993, TH1 and TH2 T-cell subsets are differentially activated by macrophages and B cells in murine leishmaniasis., Infect Immun, Vol: 61, Pages: 2266-2269, ISSN: 0019-9567
The role of antigen-presenting cells in the differential expansion of TH1 and TH2 T cells in murine leishmaniasis was investigated. In general, macrophages preferentially induced gamma interferon and interleukin-2 secretion by syngeneic Leishmania-specific T cells, whereas B cells were more efficient in activating interleukin 4 production. B cells from susceptible BALB/c mice were better in inducing TH2 responses than B cells from resistant C57BL/6 mice, whereas macrophages from C57BL/6 mice were superior to BALB/c macrophages in inducing TH1 responses.
Louis J, Rosat J P, Frith U, et al., 1993, T cell subsets triggered by L. major in mice: Study of their effector functions and of some parameters influencing their differentiation, Mem. Inst., Vol: 88 supl, Pages: 44-45
Müller I, 1992, Role of T cell subsets during the recall of immunologic memory to Leishmania major., Eur J Immunol, Vol: 22, Pages: 3063-3069, ISSN: 0014-2980
The contributions of different T cell subpopulations to the maintenance of immunity during secondary Leishmania major infections were analyzed in healed, resistant animals by depletion of T cell subsets in vivo. The strong delayed-type hypersensitivity mounted in immune genetically resistant mice upon challenge with viable promastigotes was mediated by both CD4+ and CD8+ T cells. Each T cell subpopulation alone contributes, although to a different extent, to the resolution of secondary lesions; both subsets, however, are required for an efficient and rapid healing of the secondary lesions and the decrease in the parasite burden in infected tissues. The results indicate that in immune, genetically resistant CBA mice, the activity of both T cell subsets is required for successful resistance to reinfection and an efficient maintenance of immunity.
Röcken M, Müller KM, Saurat JH, et al., 1992, Central role for TCR/CD3 ligation in the differentiation of CD4+ T cells toward A Th1 or Th2 functional phenotype., J Immunol, Vol: 148, Pages: 47-54, ISSN: 0022-1767
Activated CD4+ T cells can be classified into distinct subsets; the most divergent among them may be considered to be the IL-2 and IFN-gamma-producing Th1 clones and the IL-4 and IL-5-producing Th2 clones. Because Th1 and Th2 clones can usually be detected only after several months of culture, we used conditions that modulate the IL-2 and IL-4 production in short term culture. Here we show that freshly isolated and subsequently in vitro-activated CD4+ T cells that were cultured for 11 days with rIL-2 and restimulated showed a IFN-gamma+ IL-2+ IL-3+ IL-4- IL-5- pattern. Because these cells were not capable of providing B cell help for IgG1, IgG2a, or IgE in an APC- and TCR-dependent T-B cell assay, they expressed a phenotype typical for most Th1 clones. In contrast, activated T cells that were cultured for 11 days with IL-2 plus a mAb to CD3 and then restimulated produced a IFN-gamma- IL-2- IL-3+ IL-4+ IL-5+ pattern. These cells were capable of providing B cell help for IgG1, IgG2a, and IgE synthesis and thus presented a phenotype typical for Th2 clones. Similar results were observed when mitogenic mAb to Thy-1.2 or to framework determinants of the alpha beta TCR were used. The induction of Th1- and Th2-like cells did not depend on the relative expression of CD44 or CD45 by the T cells before activation in vitro. Because the incubation of activated T cells with anti-CD3/TCR mAb induced high unrestricted lymphokine production, the latter might be responsible for the Th2-like lymphokine pattern observed after restimulation. To address this point, TCR V beta 8+ and V beta 8- T cell blasts were co-cultured in the presence of mAb to V beta 8. After restimulation, V beta 8+ cells had a IL-4high IL-2low phenotype and V beta 8- cells had a IL-4low IL-2high phenotype. This demonstrates that TCR ligation but not lymphokines alone are capable of inducing Th2-like cells, and this points out a central role for the TCR in the generation of T cell subsets.
Müller I, Fruth U, Louis JA, 1992, Immunobiology of experimental leishmaniasis., Med Microbiol Immunol, Vol: 181, Pages: 1-12, ISSN: 0300-8584
Self-cure versus uncontrolled disease progression in experimental murine cutaneous leishmaniasis depends upon a delicate interplay among various activated cells of the host's immune system. Susceptibility or resistance to infection with Leishmania major is correlated with the ability of different inbred strains of mice to produce the characteristic spectra of lymphokines upon infection. Appropriate experimental interventions now allow the modulation of these responses, providing the possibility to render genetically susceptible mice resistant to infection and, vice versa, to cause genotypically "healer" strains to express a "non-healer" phenotype. These experimental manipulations have proven to be powerful tools in the dissection of the underlying immune mechanisms and cellular parameters responsible for susceptibility and resistance, and will perhaps allow the identification of molecules of parasite origin that induce deleterious immune responses to infection with Leishmania, and thus to exclude them from future vaccines. More importantly, rational immune intervention could permit the diversion of established host-damaging immune responses to host-protective immunization.
Muller I, Kropf P, Milon G, et al., 1992, CD8+ T lymphocytes in experimental murine cutaneous leishmaniasis, New advances on cytokines, Editors: Romagnani, Mosmann, Abbas, Publisher: Raven Press, Pages: 265-270
Louis J A, Fruth J P, Rosat F, et al., 1992, The analysis of the function and specificity of T cells triggered during infection with Leishmania, its importance for the rational dsign of a vaccine, Progress in Immunology (8th International Congress of Immunology), Pages: 775-782
Müller I, Pedrazzini T, Kropf P, et al., 1991, Establishment of resistance to Leishmania major infection in susceptible BALB/c mice requires parasite-specific CD8+ T cells., Int Immunol, Vol: 3, Pages: 587-597, ISSN: 0953-8178
Although CD4+ T cells are generally accepted to be responsible for the determination of resistance to infection in experimental murine cutaneous leishmaniasis, a contribution of CD8+ lymphocytes to immunity can be demonstrated under certain well-defined conditions. Normally highly susceptible BALB/c mice can be rendered resistant to infection with Leishmania major promastigotes by a single injection of monoclonal anti-CD4 antibodies at the beginning of infection. Mice treated in such a way can heal their primary cutaneous lesions and acquire immunity to subsequent challenge infection. Both the resolution of the primary infection and the induced state of immunity to reinfection in these mice is shown to be dependent upon the anti-leishmanial effector functions of CD8+ T cells. Furthermore, in contrast to control infected BALB/c mice, which are unable to mount a delayed-type hypersensitivity (DTH) response to viable parasites, mice cured as a result of treatment with anti-CD4 antibodies in vivo exhibit a strong DTH response, which can be significantly reduced by injection of either anti-CD4 or anti-CD8 monoclonal antibodies prior to antigenic challenge with viable promastigotes. Moreover, increased numbers of specific CD8+ T cells, able to transfer Leishmania-specific DTH responses, were found in lymphoid organs of BALB/c mice rendered resistant to infection by immunointervention with anti-CD4 monoclonal antibodies at the beginning of infection. Neutralization in vivo of interleukin 4 during the course of infection in BALB/c mice also enables these otherwise susceptible mice to resolve their cutaneous lesions and to decrease the parasite burden in infected tissues. CD8+ T cells are required for both of these beneficial effects. Taken together, these results indicate that in the immune BALB/c mouse, as in the normally resistant CBA mouse, CD8+ lymphocytes are involved in the elimination of L. major and in the establishment and maintenance of immunity against infection
Titus RG, Müller I, Kimsey P, et al., 1991, Exacerbation of experimental murine cutaneous leishmaniasis with CD4+ Leishmania major-specific T cell lines or clones which secrete interferon-gamma and mediate parasite-specific delayed-type hypersensitivity., Eur J Immunol, Vol: 21, Pages: 559-567, ISSN: 0014-2980
Leishmania major-specific T cell lines were derived from mice sensitized to the parasite. The cells were of the CD4+ T cell lineage and, upon adoptive transfer, were found to be capable of inducing parasite-specific delayed-type hypersensitivity. Adoptive transfer of these L. major-specific T cells to syngeneic recipients which were either normal, T cell deficient or B cell and antibody deficient led to exacerbation of infection upon subsequent challenge with L. major. This suggested that host T cells, B cells and antibody were not required for the L. major-specific T cells to exert their exacerbative effect on the course of cutaneous leishmaniasis. Additional studies revealed that the adoptive transfer of graded doses of these L. major-specific T cells always resulted in exacerbation of infection. Study of the localization pattern of the cells following transfer showed that they migrate preferentially to the site of the lesions. Furthermore, although the induction phase of this phenomenon was immunologically specific, its effector phase was not. Finally, T cell clones were derived from the L. major-specific T cell lines. The T cell clones were phenotypically and functionally identical to the T cell lines from which they were derived. Adoptive transfer of these parasite-specific T cell clones to normal syngeneic recipients induced an exacerbated course of infection with L. major. Interestingly, when these cloned T cells were specifically activated in vitro, the cells produced interleukin 2 and interferon-gamma, but no interleukin 4, indicating that they belong to the murine Th1 subset of CD4+ T cells.
Müller I, Milon G, Louis J, 1991, T-cell responses during infections with Leishmania major., Behring Inst Mitt, Pages: 80-83, ISSN: 0301-0457
Del Giudice G, Grillot D, Rénia L, et al., 1990, Peptide-primed CD4+ cells and malaria sporozoites., Immunol Lett, Vol: 25, Pages: 59-63, ISSN: 0165-2478
We have mapped a T cell epitope in the circumsporozoite (CS) protein of the murine malaria parasite, Plasmodium yoelii. A 21-mer synthetic peptide corresponding to the amino acid positions 59-79 (referred to as Py1), induced specific proliferation in BALB/c and C57BL/6 mice, and provided help for the production of antibodies to peptides from the repetitive region, (QGPGAP)n, of the same CS protein, when mice were immunized with the Py1 peptide conjugated to the repetitive peptide. Long-term CD3+CD4+CD8-TCR alpha beta+ T cell lines and clones were derived from both strains of mice. These lines and clones, that proliferated in an MHC-restricted fashion, did not recognize peptides from the homologous region of another murine malaria parasite, P. berghei. About 50% of these clones produced detectable amounts of IFN-gamma and IL-2, whereas the remaining produced IL-4, IL-5, and IL-6. In preliminary experiments, some of these clones specifically inhibited P. yoelii sporozoite development in vitro and conferred protection in vivo in passive transfer experiments. These findings show that heterogenous T cell populations are activated in mice upon immunization with a short peptide from the P. yoelii CS protein and that some of these cells could be active in the effector arm of the immune response against malaria sporozoites.
Grillot D, Michel M, Müller I, et al., 1990, Immune responses to defined epitopes of the circumsporozoite protein of the murine malaria parasite, Plasmodium yoelii., Eur J Immunol, Vol: 20, Pages: 1215-1222, ISSN: 0014-2980
We have investigated the immunogenicity of defined sequences of the circumsporozoite (CS) protein of the murine malaria parasite, Plasmodium yoelii. A 21-ner synthetic peptide from the nonrepetitive region of the CS protein (position 59-79, referred to as Py1) induced T cell proliferative responses in H-2d and, to a lesser extent, in H-2b mice. Conversely, a synthetic peptide (referred to as Py4) consisting of four (QGPGAP) repeats of the P. yoelii CS protein, induced an antibody response only in H-2b mice. No antibody response was observed when the Py3 peptide, consisting of three (QGPGAP) repeats, was used as an immunogen. When cross-linked to the Py4 repetitive peptide, the Py1 sequence behaved as a T helper epitope allowing the production of anti-Py4 antibodies in H-2d mice. Several long-term T cell lines and clones specific for the nonrepetitive Py1 peptide were originated in vitro from both H-2d and H-2b mice. These lines and clones were CD4+ and proliferated in a major histocompatibility complex-restricted fashion. Furthermore, Py1-specific T cell lines and clones did not proliferate in the presence of synthetic peptides from an analogous region of another rodent malaria parasite, P. berghei, despite the high degree of homology existing in this sequence of the two CS proteins. Finally, supernatants from 7 out of 13 clones (from BALB/c mice) produced detectable amounts of interleukin 2 and interferon-gamma; whereas supernatants from the 4 clones from C57BL/6 and 2 from BALB/c mice contained detectable amounts of interleukin 5. These results show that functionally heterogenous CD4+ T cell populations, belonging to either TH1 or TH2 subset, are activated upon immunization of mice with the P. yoelii Py1 synthetic peptide. It is not yet known what differential role these CD4+ subsets play during the malaria infection or after immunization with different malaria T cell epitopes. This knowledge may have a particular impact in the design of effective subunit vaccines
Müller I, Garcia-Sanz JA, Titus R, et al., 1989, Analysis of the cellular parameters of the immune responses contributing to resistance and susceptibility of mice to infection with the intracellular parasite, Leishmania major., Immunol Rev, Vol: 112, Pages: 95-113, ISSN: 0105-2896
Although the course of infection induced by L.major in mice is influenced by several factors, including the parasite virulence, the macrophage permissiveness to this parasite and response to T cell-produced lymphokines, this review has been restricted to summarizing, the recent data concerning the T-cell responses generated during infection and their effect on the disease process. Experimental evidence strongly suggests that T-cell responses play a fundamental role in resistance and susceptibility of mice to infection with L.major. It appears that resolution of lesion and exacerbation of disease result from the activity of distinct specific CD4+ T cells. There is a consensus of opinion that CD4+ T cells from the TH1 functional phenotype are generally endowed with protective function through their secreted lymphokines (e.g. IFN-gamma). However, some evidence exists that other lymphokines (e.g. TNF) might be involved in resolution of lesions. Results exist which indicate that some TH1 CD4+ T cells also contribute to susceptibility to infection. Their specificity differs from that of protective TH1 cells in the sense that these T cells might recognize parasite antigens not appropriately presented by parasitized macrophages and therefore, although releasing IFN-gamma, would not be able to concentrate this lymphokine on the surface of macrophages containing multiplying L.major. It appears that parasite-specific TH2 cells play an important role, through the IL-4 that they produce, in the severe disease seen in BALB/c mice. Determining the mechanisms responsible for the expansion of TH2 cells in genetically susceptible mice as well as assessing whether or not some parasite antigens are preferentially recognized by TH1 and TH2 cells are areas of investigation of prime importance for the rational design of a vaccine against leishmaniasis. Several observations indicate that CD8+ T cells have a role in the resolution of lesions induced by this parasite. Precise investigation o
Müller I, Louis JA, 1989, Immunity to experimental infection with Leishmania major: generation of protective L3T4+ T cell clones recognizing antigen(s) associated with live parasites., Eur J Immunol, Vol: 19, Pages: 865-871, ISSN: 0014-2980
Exacerbation and resolution of lesions induced by Leishmania major promastigotes are, at least in part, the result of the activity of distinct parasite-specific L3T4+ T lymphocytes. The present report describes L. major-specific cloned L3T4+ T lymphocytes capable of transferring substantial protective immunity to normal highly susceptible BALB/c mice. The two protective T cell clones analyzed appear to recognize antigen associated only with live L. major parasites. Therefore, the pattern of antigen reactivity of these protective T cell clones is different from that of the previously described parasite-specific L3T4+ T cells which contribute to exacerbation of disease. The results presented in this report indicate that the two opposite effects of parasite-specific L3T4+ T cells on the disease process could be mediated by functionally similar L3T4+ T cells differing in their antigen specificity.
Farrell JP, Muller I, Louis JA, 1989, A role for Lyt-2+ T cells in resistance to cutaneous leishmaniasis in immunized mice., J Immunol, Vol: 142, Pages: 2052-2056, ISSN: 0022-1767
The role of Lyt-2+ T cells in immunologic resistance to cutaneous leishmaniasis was analyzed by comparing infection patterns in resistant C57BL/6 mice and susceptible BALB/c mice induced to heal their infections after sub-lethal irradiation or i.v. immunization, with similar mice treated in vivo with anti-Lyt-2 antibodies. Administration of anti-Lyt-2 mAb resulted in a dramatic reduction in the number of lymphoid cells expressing the Lyt-2+ phenotype. Such treatment led to enhanced disease in both resistant C57BL/6 and irradiated BALB/c mice, as assessed by lesion size, but did not affect the capacity of these mice to ultimately resolve their infections. In contrast, anti-Lyt-2 treatment totally blocked the induction of resistance in i.v. immunized mice. These results suggest, that Lyt-2+ T cells may play a role in immunity to a Leishmania major infection and that their relative importance to resistance may depend on how resistance is induced.
Louis J A, Muller I, 1989, Experimental infection of mice with Leishmania major: Analysis of the role of T cells in resistance and susceptibility, Progress in Immunology, Editors: Melchers, Berlin, Publisher: Springer Verlag, Pages: 971-978
Muller I, Titus R, Caldumbide I, et al., 1989, T cell responses in resistance and susceptibility to experimental infection with Leishmania major, Frontiers of infectious diseases "New strategies in Parasitology, Editors: Adam, al, London, Publisher: Churchill Livingston, Pages: 158-175
Müller I, Pedrazzini T, Farrell JP, et al., 1989, T-cell responses and immunity to experimental infection with leishmania major., Annu Rev Immunol, Vol: 7, Pages: 561-578, ISSN: 0732-0582
Muller I, Pedrazzini T, Louis J A, 1989, Importance of specific T cell responses in experimental leishmaniasis, Immune disorders and opportunistic infections, Local Immunity, Editors: Revillard, Wierzbicki, Suresnes, France, Publisher: Fondation Franco-Allemande, Pages: 140-146
Müller I, Pedrazzini T, Louis JA, 1988, Experimentally induced cutaneous leishmaniasis: are L3T4+ T cells that promote parasite growth distinct from those mediating resistance?, Immunol Lett, Vol: 19, Pages: 251-259, ISSN: 0165-2478
A considerable body of evidence from various laboratories indicates that specific T cell responses generated during infection with Leishmania parasites play an important role both in the resolution and progression of cutaneous leishmaniasis. Recent data, summarized in this article, indicate that resolution of lesions and promotion of disease not only result from the activity of functionally distinct parasite-specific L3T4+ T cells but could also be mediated by functionally similar L3T4+ T cells differing only in their fine antigenic specificity. This contention is based on observations which suggests that (a) the induction of T cell tolerance to parasite antigens present during the early phase of infection is beneficial to the host, and (b) the specificity of L3T4+ T cell lines and clones capable of exacerbating the development of lesions is different from that of T cells mediating protection.
Muller I, Pedrazzini T, Louis J A, 1988, Specific T cell responses in experimental leishmaniasis, Topics in immunology. Ninth European Meeting., Editors: Aiuti, Bonomo, Danieli, Rome, Italy, Publisher: Il pensiero scientifico editore, Pages: 169-179
Kaufmann, S H E, Flesch I, et al., 1988, Macrophages, helper T cells and cytolytic T cells: Possible contribution to host defense against mycobacteria, Bacteria-host cell interaction, Editors: Horwitz, New York, Publisher: Alan R Liss Inc., Pages: 311-325
Müller I, Cobbold SP, Waldmann H, et al., 1987, Impaired resistance to Mycobacterium tuberculosis infection after selective in vivo depletion of L3T4+ and Lyt-2+ T cells., Infect Immun, Vol: 55, Pages: 2037-2041, ISSN: 0019-9567
The resistance of mice against Mycobacterium tuberculosis infection after selective in vivo depletion of L3T4+ and Lyt-2+ T cells was studied. Thymectomized mice were treated with rat monoclonal antibodies against the L3T4 or Lyt-2 molecule to selectively eliminate the respective T-cell subset. In both L3T4+ and Lyt-2+ T-cell-depleted mice, resistance against subsequent infection with M. tuberculosis was markedly impaired compared with that in untreated controls, with L3T4+ T-cell-depleted mice showing more pronounced effects. Simultaneous depletion of L3T4+ and Lyt-2+ T cells did not further exacerbate infection. These findings suggest that both L3T4+ and Lyt-2+ T cells are involved in the acquisition of resistance against tuberculosis.
Louis JA, Pedrazzini T, Titus RG, et al., 1987, Subsets of specific T cells and experimental cutaneous leishmaniasis., Ann Inst Pasteur Immunol, Vol: 138, Pages: 755-758, ISSN: 0769-2625
Müller I, Maier B, Brinkmann V, et al., 1986, Autoreactive T cell clones from mice infected with Mycobacterium bovis, strain Bacillus Calmette-Guérin (BCG). I. Phenotype, specificity and in vitro function., Immunobiology, Vol: 171, Pages: 366-380, ISSN: 0171-2985
Mice were infected with the intracellular microorganism, Mycobacterium bovis BCG, and draining lymph node cells were collected. A T cell line was established which was cultured in the presence of syngeneic accessory cells (AC) and killed BCG. Stimulation of this line depended on syngeneic accessory cells and did not require BCG as a source of antigen, indicating that it was autoreactive. T cell clones derived from this line had the L3T4 helper/inducer phenotype and reacted with self-Ia on syngeneic macrophages or B cell blasts. Cloned T cells were also stimulated by syngeneic accessory cells pretreated with the lysosomotropic agent chloroquine and by H-2 compatible, background gene disparate, accessory cells, suggesting that they were specific for self-Ia. After in vitro stimulation, the T cell clones secreted interleukin 2 (IL 2) and interferon-gamma (IFN-gamma), helped B cells in antibody production and activated macrophages for secretion of reactive oxygen metabolites.
Kaufmann, S H E, Eichmann K, et al., 1986, Protection against Listeria monocytogenes with a clonotypic antiserum, Leukocytes and host defense, Editors: Oppenheim, Jacobs, New York, Publisher: Alan R Liss, Pages: 331-336
Muller I, Rolink A, Freudenberg N, et al., 1986, Biological functions in vitro and in vivo of cloned autoreactive T cells from Mycobacterium bovis BCG infected mice, Leukocytes and host defense, Editors: Oppenheim, Jacobs, New York, Publisher: Alan R. Liss Inc, Pages: 325-330
Müller I, Kaufmann SH, 1985, Antigen-reactivity pattern of T-cell hybridomas from Mycobacterium bovis BCG-infected mice., Infect Immun, Vol: 49, Pages: 838-840, ISSN: 0019-9567
Lymph node cells from mice infected with live Mycobacterium bovis BCG were fused with BW5147 cells after short-term culturing in vitro. Both mycobacterium- and self-reactive T-cell hybridomas were identified. Some T-cell hybridoma clones displayed dual reactivity to self and to self plus mycobacterial antigen but did so to a different degree, indicating that infection with mycobacteria stimulates autoreactive immune responses.
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