scholarly journals Priming of a β-Galactosidase (β-GAL)-Specific Type 1 Response in BALB/c Mice Infected with β-GAL-Transfected Leishmania major

2000 ◽  
Vol 68 (2) ◽  
pp. 809-814 ◽  
Author(s):  
Hrishekesh R. Chakkalath ◽  
Afzal A. Siddiqui ◽  
Anuraj H. Shankar ◽  
Deborah E. Dobson ◽  
Stephen M. Beverley ◽  
...  
Keyword(s):  
T Cell ◽  
Leishmania Major ◽  
T Cell Response ◽  
Cd4 T Cell ◽  
Interleukin 4 ◽  
Th2 Response ◽  
C3h Mice ◽  
Ifn Γ ◽  
T Cell Lines

ABSTRACT To determine whether an ongoing response to Leishmania major would affect the response to a non-cross-reacting, non-leishmanial antigen, susceptible BALB/c mice and resistant C3H mice were infected with L. major parasites expressingEscherichia coli β-galactosidase (β-GAL); this parasite was designated L. major-βGAL. BALB/c and C3H mice responded to infection with L. major-βGAL by mounting a CD4 T-cell response to both parasite antigens and to the reporter antigen, β-GAL. The phenotypes of these T cells were characterized after generating T-cell lines from infected mice. As expected, BALB/c mice responded to infection with L. major-βGAL by producing interleukin 4 in response to the parasite and C3H mice produced gamma interferon (IFN-γ) in response to the parasite and β-GAL. Interestingly, however, BALB/c mice produced IFN-γ in response to β-GAL. Taken together, these results demonstrate that priming of IFN-γ-producing cells can occur in BALB/c mice despite the fact the animals are simultaneously mounting a potent Th2 response toL. major.

scholarly journals Enteral Immunization with Attenuated Recombinant Listeria monocytogenes as a Live Vaccine Vector: Organ-Dependent Dynamics of CD4 T Lymphocytes Reactive to a Leishmania major Tracer Epitope

2003 ◽  
Vol 71 (3) ◽  
pp. 1083-1090 ◽  
Author(s):  
Hélène Saklani-Jusforgues ◽  
Elisabeth Fontan ◽  
Neirouz Soussi ◽  
Geneviève Milon ◽  
Pierre L. Goossens
Keyword(s):  
T Cells ◽  
Listeria Monocytogenes ◽  
T Cell ◽  
Cd4 T Cells ◽  
Leishmania Major ◽  
Cd4 T Cell ◽  
Interleukin 4 ◽  
Cell Immune Response ◽  
Mesenteric Lymph Nodes ◽  
Ifn Γ

ABSTRACT Listeria monocytogenes is considered as a potential live bacterial vector, particularly for the induction of CD8 T cells. The CD4 T-cell immune response triggered after enteral immunization of mice has not yet been thoroughly characterized. The dynamics of gamma interferon (IFN-γ)- and interleukin-4 (IL-4)-secreting CD4 T cells were analyzed after priming through intragastric delivery of an attenuated ΔactA recombinant L. monocytogenes strain expressing the Leishmania major LACK protein; a peptide of this protein, LACK158-173 peptide (pLACK), is a well-characterized CD4 T-cell target in BALB/c mice. Five compartments were monitored: Peyer's patches, mesenteric lymph nodes (MLN), spleen, liver, and blood. A single intragastric inoculation of ΔactA-LACK-LM in BALB/c mice led to colonization of the MLN and spleen at a significant level for at least 3 days. Efficient priming of IFN-γ-secreting pLACK-reactive CD4 T cells was observed in all tested compartments. Interestingly, IL-4-secreting pLACK-reactive CD4 T cells were detectable at day 6 or 7 only in blood and liver. The absence of translocation of viable bacteria through the intestinal epithelium after further ΔactA-LACK-LM inoculations was concomitant with the absence of an increase in the level of IFN-γ secreted by the MLN, blood, and splenic pLACK-reactive Th1 T cells, although the levels remained significantly above the basal level. No change in this population size was detected in the spleen. However, an increase in the number of intragastric inoculations had a clinical beneficial effect in L. major-infected BALB/c mice. L. monocytogenes thus presents the potential of an efficient vector for induction of CD4 T cells when administered by the enteral route.

scholarly journals Cytokine Induction by Streptococcus mutans and Pulpal Pathogenesis

2000 ◽  
Vol 68 (12) ◽  
pp. 6785-6789 ◽  
Author(s):  
Chin-Lo Hahn ◽  
Al M. Best ◽  
John G. Tew
Keyword(s):  
T Cells ◽  
T Cell ◽  
Streptococcus Mutans ◽  
Plasma Cells ◽  
Mrna Level ◽  
T Cell Response ◽  
Interleukin 4 ◽  
Peripheral Blood Mononuclear ◽  
Ifn Γ

ABSTRACT Chronic pulpal inflammation under caries appears to be elicited by bacterial antigens that diffuse into the pulp through dentinal tubules. This prompted the hypothesis that cytokines elicited by antigens fromStreptococcus mutans, which frequently dominates shallow lesions, could play a major role in eliciting the initial T-cell response in the pulp. To test this, we examined the ability of S. mutans to stimulate T cells and elicit cytokines and usedLactobacillus casei, which often predominates in deep carious lesions where B cells and plasma cells predominate, as a control. In addition, the presence of cytokines in the pulp was analyzed at the mRNA level. S. mutans elicited potent gamma interferon (IFN-γ) responses in peripheral blood mononuclear cell cultures and reduced the CD4/CD8 ratio by promoting CD8+ T cells. Multiple inflammatory cytokine mRNAs (IFN-γ, interleukin 4 [IL-4], and IL-10) were detected in human dental pulp. A higher prevalence of IFN-γ (67%) than IL-4 (19%) or IL-10 (29%) was obtained in shallow caries, suggesting a type 1 cytokine mechanism in early pulpitis where S. mutanspredominates. In contrast, in deep caries no differences in cytokine frequency were observed. Furthermore, the presence of IFN-γ in the pulp correlated with the presence of S. mutans. The extraordinary induction of type 1 cytokines and the preferential activation of CD8+ T cells by S. mutans offers an explanation for the etiology of the CD8+ T-cell-dominant lesion in early pulpitis and suggests that S. mutans may have a major impact on the initial lesion and pulpal pathology.

scholarly journals An Adaptive Chlamydia trachomatis-Specific IFN-γ-Producing CD4+ T Cell Response Is Associated With Protection Against Chlamydia Reinfection in Women

2018 ◽  
Vol 9 ◽  
Author(s):  
Rakesh K. Bakshi ◽  
Kanupriya Gupta ◽  
Stephen J. Jordan ◽  
Xiaofei Chi ◽  
Shelly Y. Lensing ◽  
...  
Keyword(s):  
T Cell ◽  
Chlamydia Trachomatis ◽  
Cell Response ◽  
T Cell Response ◽  
Cd4 T Cell ◽  
Ifn Γ

scholarly journals Characterization of an I-E-Restricted, gp63-Specific, CD4-T-Cell Clone from Leishmania major-Resistant C3H Mice That Secretes Type 2 Cytokines and Exacerbates Infection with L. major

2004 ◽  
Vol 72 (8) ◽  
pp. 4486-4493
Author(s):  
Cynthia M. Theodos ◽  
Robin V. Morris ◽  
Jeanette V. Bishop ◽  
Jeremy D. Jones ◽  
W. Robert McMaster ◽  
...  
Keyword(s):  
T Cell ◽  
Leishmania Major ◽  
Transforming Growth Factor ◽  
Cell Clone ◽  
Parasite Burden ◽  
Cd4 T Cell ◽  
Amino Terminal ◽  
T Cell Clone ◽  
C3h Mice

ABSTRACT A T-cell clone (designated KLmB-3) was derived from resistant C3H mice 2 weeks after infection with Leishmania major. KLmB-3 was a CD4-T-cell clone that utilized the Vβ8.1 T-cell receptor. When adoptively transferred to naive C3H mice, KLmB-3 unexpectedly exacerbated infection with L. major (it increased the cutaneous lesion size and the parasite burden within the lesion). The ability of KLmB-3 to exacerbate disease correlated with its ability to produce the type 2-associated cytokines interleukin-4 (IL-4), IL-5, IL-10, and transforming growth factor beta. Interestingly, KLmB-3 was specific for an epitope in the amino-terminal end of the L. major surface gp63 zinc metalloproteinase (leishmanolysin) that has been shown to be capable of inducing a protective immune response. Moreover, KLmB-3 was activated when this epitope was presented in the context of H-2 I-E rather than H-2 I-A.

scholarly journals Borrelia burgdorferi activates a T helper type 1-like T cell subset in Lyme arthritis.

1991 ◽  
Vol 174 (3) ◽  
pp. 593-601 ◽  
Author(s):  
H Yssel ◽  
M C Shanafelt ◽  
C Soderberg ◽  
P V Schneider ◽  
J Anzola ◽  
...  
Keyword(s):  
T Cell ◽  
Borrelia Burgdorferi ◽  
Cell Subset ◽  
Chronic Inflammatory Disease ◽  
T Cell Response ◽  
Lyme Arthritis ◽  
T Helper ◽  
Cell Clones ◽  
T Cell Lines

18 cloned T cell lines reactive with Borrelia burgdorferi proteins, all CD3+4+8-TCR-alpha/beta+ and restricted by HLA class II proteins, were isolated from four patients with chronic Lyme arthritis. Analysis of these T cell clones indicated that the T cell response to the Lyme disease spirochete is not oligoclonally restricted; yet all produced the same pattern of lymphokines, resembling that of murine type 1 T helper cells, after antigen-specific or nonspecific stimulation. Therefore, a subset of human CD4+ T cells, with a distinct profile of lymphokine secretion, is selectively activated by the pathogen inciting this chronic inflammatory disease.

Rapid establishment of a stable IL-4/IFN-γ production profile in the antigen-specific CD4+ T cell response to protein immunization

1994 ◽  
Vol 6 (10) ◽  
pp. 1515-1523 ◽  
Author(s):  
Anne Kelso ◽  
Penny Groves ◽  
Anthony B. Troutt ◽  
Michael H. Pech
Keyword(s):  
T Cell ◽  
Cell Response ◽  
T Cell Response ◽  
Cd4 T Cell ◽  
Ifn Γ ◽  
Protein Immunization

scholarly journals CD11c depletion severely disrupts Th2 induction and development in vivo

2010 ◽  
Vol 207 (10) ◽  
pp. 2089-2096 ◽  
Author(s):  
Alexander T. Phythian-Adams ◽  
Peter C. Cook ◽  
Rachel J. Lundie ◽  
Lucy H. Jones ◽  
Katherine A. Smith ◽  
...  
Keyword(s):  
T Cell ◽  
Helminth Infection ◽  
Vital Role ◽  
Cd4 T Cell ◽  
Th2 Response ◽  
Cell Responses ◽  
Ifn Γ ◽  
Antigen Presenting ◽  
Th2 Development

Although dendritic cells (DCs) are adept initiators of CD4+ T cell responses, their fundamental importance in this regard in Th2 settings remains to be demonstrated. We have used CD11c–diphtheria toxin (DTx) receptor mice to deplete CD11c+ cells during the priming stage of the CD4+ Th2 response against the parasitic helminth Schistosoma mansoni. DTx treatment significantly depleted CD11c+ DCs from all tissues tested, with 70–80% efficacy. Even this incomplete depletion resulted in dramatically impaired CD4+ T cell production of Th2 cytokines, altering the balance of the immune response and causing a shift toward IFN-γ production. In contrast, basophil depletion using Mar-1 antibody had no measurable effect on Th2 induction in this system. These data underline the vital role that CD11c+ antigen-presenting cells can play in orchestrating Th2 development against helminth infection in vivo, a response that is ordinarily balanced so as to prevent the potentially damaging production of inflammatory cytokines.

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