scholarly journals IL-4 Rapidly Produced by Vβ4 Vα8 CD4+ T Cells Instructs Th2 Development and Susceptibility to Leishmania major in BALB/c Mice

Immunity ◽  
1997 ◽  
Vol 6 (5) ◽  
pp. 541-549 ◽  
Author(s):  
Pascal Launois ◽  
Ivan Maillard ◽  
Sabine Pingel ◽  
Kristin G. Swihart ◽  
Ioannis Xénarios ◽  
...  
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Leishmania Major ◽  
Th2 Development

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 Primed Antigen-Specific CD4+ T Cells Are Required for NK Cell Activation In Vivo upon Leishmania major Infection

2010 ◽  
Vol 185 (4) ◽  
pp. 2174-2181 ◽  
Author(s):  
Franck Bihl ◽  
Julien Pecheur ◽  
Béatrice Bréart ◽  
Gwenola Poupon ◽  
Julie Cazareth ◽  
...  
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Cell Activation ◽  
Leishmania Major ◽  
Nk Cell ◽  
Major Infection

scholarly journals Friend of GATA-1 Represses GATA-3–dependent Activity in CD4+ T Cells

2001 ◽  
Vol 194 (10) ◽  
pp. 1461-1471 ◽  
Author(s):  
Meixia Zhou ◽  
Wenjun Ouyang ◽  
Qian Gong ◽  
Samuel G. Katz ◽  
J. Michael White ◽  
...  
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Th2 Cells ◽  
T Helper ◽  
Naive T Cells ◽  
Naïve T Cells ◽  
Gata Transcription Factor ◽  
Dependent Activity ◽  
Th2 Development ◽  
Primary Activation

The development of naive CD4+ T cells into a T helper (Th) 2 subset capable of producing interleukin (IL)-4, IL-5, and IL-13 involves a signal transducer and activator of transcription (Stat)6-dependent induction of GATA-3 expression, followed by Stat6-independent GATA-3 autoactivation. The friend of GATA (FOG)-1 protein regulates GATA transcription factor activity in several stages of hematopoietic development including erythrocyte and megakaryocyte differentiation, but whether FOG-1 regulates GATA-3 in T cells is uncertain. We show that FOG-1 can repress GATA-3–dependent activation of the IL-5 promoter in T cells. Also, FOG-1 overexpression during primary activation of naive T cells inhibited Th2 development in CD4+ T cells. FOG-1 fully repressed GATA-3–dependent Th2 development and GATA-3 autoactivation, but not Stat6-dependent induction of GATA-3. FOG-1 overexpression repressed development of Th2 cells from naive T cells, but did not reverse the phenotype of fully committed Th2 cells. Thus, FOG-1 may be one factor capable of regulating the Th2 development.

scholarly journals Skin-resident CD4+ T cells protect against Leishmania major by recruiting and activating inflammatory monocytes

2017 ◽  
Vol 13 (4) ◽  
pp. e1006349 ◽  
Author(s):  
Nelson D. Glennie ◽  
Susan W. Volk ◽  
Phillip Scott
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Leishmania Major ◽  
Inflammatory Monocytes

scholarly journals Selective Activation and Expansion of High-Affinity CD4+ T Cells in Resistant Mice upon Infection with Leishmania major

Immunity ◽  
2000 ◽  
Vol 13 (6) ◽  
pp. 771-782 ◽  
Author(s):  
Laurent Malherbe ◽  
Christophe Filippi ◽  
Valérie Julia ◽  
Gilles Foucras ◽  
Monica Moro ◽  
...  
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Leishmania Major ◽  
Selective Activation ◽  
High Affinity

scholarly journals Leishmania promastigotes evade interleukin 12 (IL-12) induction by macrophages and stimulate a broad range of cytokines from CD4+ T cells during initiation of infection.

1994 ◽  
Vol 179 (2) ◽  
pp. 447-456 ◽  
Author(s):  
S L Reiner ◽  
S Zheng ◽  
Z E Wang ◽  
L Stowring ◽  
R M Locksley
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Leishmania Major ◽  
Interleukin 12 ◽  
Insect Vector ◽  
T Helper 1 ◽  
Ifn Gamma ◽  
Effector Cells

Leishmania major are intramacrophage parasites whose eradication requires the induction of T helper 1 (Th1) effector cells capable of activating macrophages to a microbicidal state. Interleukin 12 (IL-12) has been recently identified as a macrophage-derived cytokine capable of mediating Th1 effector cell development, and of markedly enhancing interferon gamma (IFN-gamma) production by T cells and natural killer cells. Infection of macrophages in vitro by promastigotes of L. major caused no induction of IL-12 p40 transcripts, whereas stimulation using heat-killed Listeria or bacterial lipopolysaccharide induced readily detectable IL-12 mRNA. Using a competitor construct to quantitate a number of transcripts, a kinetic analysis of cytokine induction during the first few days of infection by L. major was performed. All strains of mice examined, including susceptible BALB/c and resistant C57BL/6, B10.D2, and C3H/HeN, had the appearance of a CD4+ population in the draining lymph nodes that contained transcripts for IL-2, IL-4, and IFN-gamma (and in some cases, IL-10) that peaked 4 d after infection. In resistant mice, the transcripts for IL-2, IL-4, and IL-10 were subsequently downregulated, whereas in susceptible BALB/c mice, these transcripts were only slightly decreased, and IL-4 continued to be reexpressed at high levels. IL-12 transcripts were first detected in vivo by 7 d after infection, consistent with induction by intracellular amastigotes. Challenge of macrophages in vitro confirmed that amastigotes, in contrast to promastigotes, induced IL-12 p40 mRNA. Reexamination of the cytokine mRNA at 4 d revealed expression of IL-13 in all strains analyzed, suggesting that IL-2 and IL-13 may mediate the IL-12-independent production of IFN-gamma during the first days after infection. Leishmania have evolved to avoid inducing IL-12 from host macrophages during transmission from the insect vector, and cause a striking induction of mRNAs for IL-2, IL-4, IL-10, and IL-13 in CD4+ T cells. Each of these activities may favor survival of the organism.

scholarly journals Skin-resident memory CD4+ T cells enhance protection against Leishmania major infection

2015 ◽  
Vol 212 (9) ◽  
pp. 1405-1414 ◽  
Author(s):  
Nelson D. Glennie ◽  
Venkata A. Yeramilli ◽  
Daniel P. Beiting ◽  
Susan W. Volk ◽  
Casey T. Weaver ◽  
...  
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Leishmania Major ◽  
Memory T Cells ◽  
Critical Role ◽  
Parasitic Infection ◽  
Dependent Manner ◽  
Peripheral Tissues ◽  
Circulating T Cells ◽  
Memory Cd4 T Cells

Leishmaniasis causes a significant disease burden worldwide. Although Leishmania-infected patients become refractory to reinfection after disease resolution, effective immune protection has not yet been achieved by human vaccines. Although circulating Leishmania-specific T cells are known to play a critical role in immunity, the role of memory T cells present in peripheral tissues has not been explored. Here, we identify a population of skin-resident Leishmania-specific memory CD4+ T cells. These cells produce IFN-γ and remain resident in the skin when transplanted by skin graft onto naive mice. They function to recruit circulating T cells to the skin in a CXCR3-dependent manner, resulting in better control of the parasites. Our findings are the first to demonstrate that CD4+ TRM cells form in response to a parasitic infection, and indicate that optimal protective immunity to Leishmania, and thus the success of a vaccine, may depend on generating both circulating and skin-resident memory T cells.

scholarly journals CD4+ T Cells Which React to the Leishmania major LACK Antigen Rapidly Secrete Interleukin-4 and Are Detrimental to the Host in Resistant B10.D2 Mice

1999 ◽  
Vol 67 (7) ◽  
pp. 3641-3644 ◽  
Author(s):  
Valérie Julia ◽  
Nicolas Glaichenhaus
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Leishmania Major ◽  
Interleukin 4 ◽  
Rapid Production

ABSTRACT Leishmania major induces the rapid production of interleukin-4 (IL-4) in both susceptible BALB/c and resistant B10.D2 mice. In both strains, IL-4 is produced by T cells which react to the parasite LACK (for Leishmania homolog of the receptor for activated C kinase) antigen. The rapid production of IL-4 in B10.D2 mice does not confer susceptibility but results in increased parasite burdens.

scholarly journals Expansion of gamma delta+ T cells in BALB/c mice infected with Leishmania major is dependent upon Th2-type CD4+ T cells.

1995 ◽  
Vol 63 (8) ◽  
pp. 3000-3004 ◽  
Author(s):  
J P Rosat ◽  
F Conceiçao-Silva ◽  
G A Waanders ◽  
F Beermann ◽  
A Wilson ◽  
...  
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Leishmania Major ◽  
Gamma Delta T Cells ◽  
Gamma Delta

scholarly journals Listeria monocytogenes as a Short-Lived Delivery System for the Induction of Type 1 Cell-Mediated Immunity against the p36/LACK Antigen of Leishmania major

2000 ◽  
Vol 68 (3) ◽  
pp. 1498-1506 ◽  
Author(s):  
Neirouz Soussi ◽  
Geneviève Milon ◽  
Jean-Hervé Colle ◽  
Evelyne Mougneau ◽  
Nicolas Glaichenhaus ◽  
...  
Keyword(s):  
T Cells ◽  
Listeria Monocytogenes ◽  
Cd4 T Cells ◽  
Leishmania Major ◽  
Ex Vivo ◽  
Experimental Models ◽  
Interleukin 4 ◽  
Cell Mediated Immunity ◽  
Th1 Cells ◽  
Ifn Γ

ABSTRACT Listeria monocytogenes has been used as an experimental live vector for the induction of CD8-mediated immune responses in various viral and tumoral experimental models. Susceptibility of BALB/c mice to Leishmania major infection has been correlated to the preferential development of Th2 CD4 T cells through an early production of interleukin 4 (IL-4) by a restricted population of CD4 T cells which react to a single parasite antigen, LACK (stands forLeishmania homologue of receptors for activated C kinase). Experimental vaccination with LACK can redirect the differentiation of CD4+ T cells towards the Th1 pathway if LACK is coadministrated with IL-12. As IL-12 is known to be induced by L. monocytogenes, we have tested the ability of a recombinant attenuated actA mutant L. monocytogenes strain expressing LACK to induce the development of LACK-specific Th1 cells in both B10.D2 and BALB/c mice, which are resistant and susceptible toL. major, respectively. After a single injection of LACK-expressing L. monocytogenes, IL-12/p40 transcripts showed a rapid burst, and peaks of gamma interferon (IFN-γ)-secreting LACK-specific Th1 cells were detected around day 5 in the spleens and livers of mice of both strains. These primed IFN-γ-secreting LACK-reactive T cells were not detected ex vivo after day 7 of immunization but could be recruited and detected 15 days later in the draining lymph node after an L. major footpad challenge. Although immunization of BALB/c mice with LACK-expressing L. monocytogenes did not change the course of the infection withL. major, immunized B10.D2 mice exhibited significantly smaller lesions than nonimmunized controls. Thus, our results demonstrate that, in addition of its recognized use for the induction of effector CD8 T cells, L. monocytogenes can also be used as a live recombinant vector to favor the development of potentially protective IFN-γ-secreting Th1 CD4 T lymphocytes.

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