Protective CD4+ Th1 cell-mediated immunity is reliant upon execution of effector function prior to the establishment of the pathogen niche
Intracellular infection with the parasite Leishmania major features a state of concomitant immunity in which CD4+ T helper 1 (Th1) cell-mediated immunity against reinfection coincides with a chronic but sub-clinical primary infection. In this setting, the rapidity of the Th1 response at a secondary...
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| Veröffentlicht in: | PLoS pathogens 2021-09, Vol.17 (9), p.e1009944-e1009944 |
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| creator | Hohman, Leah S Mou, Zhirong Carneiro, Matheus B Ferland, Gabriel Kratofil, Rachel M Kubes, Paul Uzonna, Jude E Peters, Nathan C |
| description | Intracellular infection with the parasite Leishmania major features a state of concomitant immunity in which CD4+ T helper 1 (Th1) cell-mediated immunity against reinfection coincides with a chronic but sub-clinical primary infection. In this setting, the rapidity of the Th1 response at a secondary site of challenge in the skin represents the best correlate of parasite elimination and has been associated with a reversal in Leishmania-mediated modulation of monocytic host cells. Remarkably, the degree to which Th1 cells are absolutely reliant upon the time at which they interact with infected monocytes to mediate their protective effect has not been defined. In the present work, we report that CXCR3-dependent recruitment of Ly6C+ Th1 effector (Th1EFF) cells is indispensable for concomitant immunity and acute ( |
| doi_str_mv | 10.1371/journal.ppat.1009944 |
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In this setting, the rapidity of the Th1 response at a secondary site of challenge in the skin represents the best correlate of parasite elimination and has been associated with a reversal in Leishmania-mediated modulation of monocytic host cells. Remarkably, the degree to which Th1 cells are absolutely reliant upon the time at which they interact with infected monocytes to mediate their protective effect has not been defined. In the present work, we report that CXCR3-dependent recruitment of Ly6C+ Th1 effector (Th1EFF) cells is indispensable for concomitant immunity and acute (<4 days post-infection) Th1EFF cell-phagocyte interactions are critical to prevent the establishment of a permissive pathogen niche, as evidenced by altered recruitment, gene expression and functional capacity of innate and adaptive immune cells at the site of secondary challenge. Surprisingly, provision of Th1EFF cells after establishment of the pathogen niche, even when Th1 cells were provided in large quantities, abrogated protection, Th1EFF cell accumulation and IFN-γ production, and iNOS production by inflammatory monocytes. These findings indicate that protective Th1 immunity is critically dependent on activation of permissive phagocytic host cells by preactivated Th1EFF cells at the time of infection.</description><identifier>ISSN: 1553-7374</identifier><identifier>ISSN: 1553-7366</identifier><identifier>EISSN: 1553-7374</identifier><identifier>DOI: 10.1371/journal.ppat.1009944</identifier><identifier>PMID: 34543348</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Antigens ; Biology and Life Sciences ; CD4 antigen ; Cell-mediated immunity ; Chemokines ; Chronic infection ; CXCR3 protein ; Effector cells ; Gene expression ; Immune system ; Immunity ; Immunity, Cellular - immunology ; Infections ; Inflammation ; Leishmania major - immunology ; Leishmaniasis, Cutaneous - immunology ; Lymphocytes ; Lymphocytes T ; Medicine and Health Sciences ; Mice ; Mice, Inbred C57BL ; Monocytes ; Monocytes - immunology ; Nitric-oxide synthase ; Parasites ; Parasitic diseases ; Pathogens ; Phagocytes ; Recruitment ; Th1 Cells - immunology ; Tropical diseases ; Vaccines ; γ-Interferon</subject><ispartof>PLoS pathogens, 2021-09, Vol.17 (9), p.e1009944-e1009944</ispartof><rights>2021 Hohman et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2021 Hohman et al 2021 Hohman et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c526t-6c2b3c7c89880eee9b2a6e4edc929a6cd08a18eb798c62cdc53367d4eb43bffe3</citedby><cites>FETCH-LOGICAL-c526t-6c2b3c7c89880eee9b2a6e4edc929a6cd08a18eb798c62cdc53367d4eb43bffe3</cites><orcidid>0000-0003-1494-4603 ; 0000-0002-2548-9581 ; 0000-0002-6520-1060 ; 0000-0003-3927-2508 ; 0000-0001-8746-7639 ; 0000-0003-2759-0664</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8483310/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8483310/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34543348$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Nakhasi, Hira L.</contributor><creatorcontrib>Hohman, Leah S</creatorcontrib><creatorcontrib>Mou, Zhirong</creatorcontrib><creatorcontrib>Carneiro, Matheus B</creatorcontrib><creatorcontrib>Ferland, Gabriel</creatorcontrib><creatorcontrib>Kratofil, Rachel M</creatorcontrib><creatorcontrib>Kubes, Paul</creatorcontrib><creatorcontrib>Uzonna, Jude E</creatorcontrib><creatorcontrib>Peters, Nathan C</creatorcontrib><title>Protective CD4+ Th1 cell-mediated immunity is reliant upon execution of effector function prior to the establishment of the pathogen niche</title><title>PLoS pathogens</title><addtitle>PLoS Pathog</addtitle><description>Intracellular infection with the parasite Leishmania major features a state of concomitant immunity in which CD4+ T helper 1 (Th1) cell-mediated immunity against reinfection coincides with a chronic but sub-clinical primary infection. In this setting, the rapidity of the Th1 response at a secondary site of challenge in the skin represents the best correlate of parasite elimination and has been associated with a reversal in Leishmania-mediated modulation of monocytic host cells. Remarkably, the degree to which Th1 cells are absolutely reliant upon the time at which they interact with infected monocytes to mediate their protective effect has not been defined. In the present work, we report that CXCR3-dependent recruitment of Ly6C+ Th1 effector (Th1EFF) cells is indispensable for concomitant immunity and acute (<4 days post-infection) Th1EFF cell-phagocyte interactions are critical to prevent the establishment of a permissive pathogen niche, as evidenced by altered recruitment, gene expression and functional capacity of innate and adaptive immune cells at the site of secondary challenge. Surprisingly, provision of Th1EFF cells after establishment of the pathogen niche, even when Th1 cells were provided in large quantities, abrogated protection, Th1EFF cell accumulation and IFN-γ production, and iNOS production by inflammatory monocytes. These findings indicate that protective Th1 immunity is critically dependent on activation of permissive phagocytic host cells by preactivated Th1EFF cells at the time of infection.</description><subject>Animals</subject><subject>Antigens</subject><subject>Biology and Life Sciences</subject><subject>CD4 antigen</subject><subject>Cell-mediated immunity</subject><subject>Chemokines</subject><subject>Chronic infection</subject><subject>CXCR3 protein</subject><subject>Effector cells</subject><subject>Gene expression</subject><subject>Immune system</subject><subject>Immunity</subject><subject>Immunity, Cellular - immunology</subject><subject>Infections</subject><subject>Inflammation</subject><subject>Leishmania major - immunology</subject><subject>Leishmaniasis, Cutaneous - immunology</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Medicine and Health Sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Monocytes</subject><subject>Monocytes - immunology</subject><subject>Nitric-oxide synthase</subject><subject>Parasites</subject><subject>Parasitic diseases</subject><subject>Pathogens</subject><subject>Phagocytes</subject><subject>Recruitment</subject><subject>Th1 Cells - immunology</subject><subject>Tropical diseases</subject><subject>Vaccines</subject><subject>γ-Interferon</subject><issn>1553-7374</issn><issn>1553-7366</issn><issn>1553-7374</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNptUttq3DAQNaWlSdP-QWkFfSmU3UqWbEsvhbK9BQLtQ_os5PF4rcW2XEkOzS_kq6PddUJSCgKNRuccnRlNlr1mdM14xT7u3OxH06-nycQ1o1QpIZ5kp6wo-KrilXj6ID7JXoSwo1Qwzsrn2QkXheBcyNPs5pd3ESHaKySbL-IDuewYAez71YCNNREbYodhHm28JjYQj701YyTz5EaCfxHmaFPkWoJtm2ScJ-08wiE5eZuO0ZHYIcEQTd3b0A2Y6Am_TybnndviSEYLHb7MnrWmD_hq2c-y39--Xm5-rC5-fj_ffL5YQZGXcVVCXnOoQCopKSKqOjclCmxA5cqU0FBpmMS6UhLKHBooOC-rRmAteJ1M8rPs7VF36l3QSxuDzguZVilynhDnR0TjzE6nOgbjr7UzVh8Szm-18dFCj1pAqVgOFLiSoqhUbWreVqqVQkHLDUtan5bX5jq1FFL53vSPRB_fjLbTW3elpZCcM5oE3i8C3v2ZUx_1YMP-h8yIbt77rgpayurg-90_0P9XJ44o8C4Ej-29GUb1frTuWHo_WnoZrUR787CQe9LdLPFbNRPP2A</recordid><startdate>20210901</startdate><enddate>20210901</enddate><creator>Hohman, Leah S</creator><creator>Mou, Zhirong</creator><creator>Carneiro, Matheus B</creator><creator>Ferland, Gabriel</creator><creator>Kratofil, Rachel M</creator><creator>Kubes, Paul</creator><creator>Uzonna, Jude E</creator><creator>Peters, Nathan C</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QL</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0003-1494-4603</orcidid><orcidid>https://orcid.org/0000-0002-2548-9581</orcidid><orcidid>https://orcid.org/0000-0002-6520-1060</orcidid><orcidid>https://orcid.org/0000-0003-3927-2508</orcidid><orcidid>https://orcid.org/0000-0001-8746-7639</orcidid><orcidid>https://orcid.org/0000-0003-2759-0664</orcidid></search><sort><creationdate>20210901</creationdate><title>Protective CD4+ Th1 cell-mediated immunity is reliant upon execution of effector function prior to the establishment of the pathogen niche</title><author>Hohman, Leah S ; Mou, Zhirong ; Carneiro, Matheus B ; Ferland, Gabriel ; Kratofil, Rachel M ; Kubes, Paul ; Uzonna, Jude E ; Peters, Nathan C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c526t-6c2b3c7c89880eee9b2a6e4edc929a6cd08a18eb798c62cdc53367d4eb43bffe3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animals</topic><topic>Antigens</topic><topic>Biology and Life Sciences</topic><topic>CD4 antigen</topic><topic>Cell-mediated immunity</topic><topic>Chemokines</topic><topic>Chronic infection</topic><topic>CXCR3 protein</topic><topic>Effector cells</topic><topic>Gene expression</topic><topic>Immune system</topic><topic>Immunity</topic><topic>Immunity, Cellular - immunology</topic><topic>Infections</topic><topic>Inflammation</topic><topic>Leishmania major - immunology</topic><topic>Leishmaniasis, Cutaneous - immunology</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>Medicine and Health Sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Monocytes</topic><topic>Monocytes - immunology</topic><topic>Nitric-oxide synthase</topic><topic>Parasites</topic><topic>Parasitic diseases</topic><topic>Pathogens</topic><topic>Phagocytes</topic><topic>Recruitment</topic><topic>Th1 Cells - immunology</topic><topic>Tropical diseases</topic><topic>Vaccines</topic><topic>γ-Interferon</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hohman, Leah S</creatorcontrib><creatorcontrib>Mou, Zhirong</creatorcontrib><creatorcontrib>Carneiro, Matheus B</creatorcontrib><creatorcontrib>Ferland, Gabriel</creatorcontrib><creatorcontrib>Kratofil, Rachel M</creatorcontrib><creatorcontrib>Kubes, Paul</creatorcontrib><creatorcontrib>Uzonna, Jude E</creatorcontrib><creatorcontrib>Peters, Nathan C</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - 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Surprisingly, provision of Th1EFF cells after establishment of the pathogen niche, even when Th1 cells were provided in large quantities, abrogated protection, Th1EFF cell accumulation and IFN-γ production, and iNOS production by inflammatory monocytes. These findings indicate that protective Th1 immunity is critically dependent on activation of permissive phagocytic host cells by preactivated Th1EFF cells at the time of infection.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>34543348</pmid><doi>10.1371/journal.ppat.1009944</doi><orcidid>https://orcid.org/0000-0003-1494-4603</orcidid><orcidid>https://orcid.org/0000-0002-2548-9581</orcidid><orcidid>https://orcid.org/0000-0002-6520-1060</orcidid><orcidid>https://orcid.org/0000-0003-3927-2508</orcidid><orcidid>https://orcid.org/0000-0001-8746-7639</orcidid><orcidid>https://orcid.org/0000-0003-2759-0664</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Antigens Biology and Life Sciences CD4 antigen Cell-mediated immunity Chemokines Chronic infection CXCR3 protein Effector cells Gene expression Immune system Immunity Immunity, Cellular - immunology Infections Inflammation Leishmania major - immunology Leishmaniasis, Cutaneous - immunology Lymphocytes Lymphocytes T Medicine and Health Sciences Mice Mice, Inbred C57BL Monocytes Monocytes - immunology Nitric-oxide synthase Parasites Parasitic diseases Pathogens Phagocytes Recruitment Th1 Cells - immunology Tropical diseases Vaccines γ-Interferon |
| title | Protective CD4+ Th1 cell-mediated immunity is reliant upon execution of effector function prior to the establishment of the pathogen niche |
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