Evidence for differential induction of helper T cell subsets during Trichinella spiralis infection

The H-2-compatible mouse strains, AKR and B10.BR, exhibit disparate responses to infection with the parasitic nematode Trichinella spiralis. The resistant AKR mice expel intestinal adult worms faster than susceptible B10.BR mice. We tested antibody and lymphokine responses in these strains. With res...

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Veröffentlicht in:The Journal of immunology (1950) 1989-12, Vol.143 (12), p.4232-4237
Hauptverfasser: Pond, L, Wassom, DL, Hayes, CE
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container_title The Journal of immunology (1950)
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creator Pond, L
Wassom, DL
Hayes, CE
description The H-2-compatible mouse strains, AKR and B10.BR, exhibit disparate responses to infection with the parasitic nematode Trichinella spiralis. The resistant AKR mice expel intestinal adult worms faster than susceptible B10.BR mice. We tested antibody and lymphokine responses in these strains. With respect to antibody responses, the B10.BR mice had 3- to 10-fold more serum IgE and T. spiralis-specific IgG1 and IgA than AKR mice. The B10.BR mice also had greater numbers of IgG and IgA plaque-forming cells than AKR mice. In contrast, AKR mice produced T. spiralis-specific IgG2a, whereas the B10.BR mice did not. The antibody response kinetics of these strains were similar. We also analyzed lymphokine secretion after restimulating lymphocytes in vitro with T. spiralis Ag. The AKR mesenteric lymph node cells produced more IFN-gamma and less IL-4 than the B10.BR mesenteric lymph node cells. The B10.BR splenocytes produced more IL-4 than the AKR splenocytes, although splenocyte IFN-gamma production was not different. The kinetics of IL-4 production also differed between the two strains. In summary, resistant AKR mice produced more IFN-gamma and T. spiralis-specific IgG2a than susceptible B10.BR mice, which produced more IL-4, IgE, and T. spiralis-specific IgG1. Our results are consistent with differential activation of Th cell subsets in T. spiralis-infected AKR and B10.BR mice.
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The resistant AKR mice expel intestinal adult worms faster than susceptible B10.BR mice. We tested antibody and lymphokine responses in these strains. With respect to antibody responses, the B10.BR mice had 3- to 10-fold more serum IgE and T. spiralis-specific IgG1 and IgA than AKR mice. The B10.BR mice also had greater numbers of IgG and IgA plaque-forming cells than AKR mice. In contrast, AKR mice produced T. spiralis-specific IgG2a, whereas the B10.BR mice did not. The antibody response kinetics of these strains were similar. We also analyzed lymphokine secretion after restimulating lymphocytes in vitro with T. spiralis Ag. The AKR mesenteric lymph node cells produced more IFN-gamma and less IL-4 than the B10.BR mesenteric lymph node cells. The B10.BR splenocytes produced more IL-4 than the AKR splenocytes, although splenocyte IFN-gamma production was not different. The kinetics of IL-4 production also differed between the two strains. In summary, resistant AKR mice produced more IFN-gamma and T. spiralis-specific IgG2a than susceptible B10.BR mice, which produced more IL-4, IgE, and T. spiralis-specific IgG1. 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The resistant AKR mice expel intestinal adult worms faster than susceptible B10.BR mice. We tested antibody and lymphokine responses in these strains. With respect to antibody responses, the B10.BR mice had 3- to 10-fold more serum IgE and T. spiralis-specific IgG1 and IgA than AKR mice. The B10.BR mice also had greater numbers of IgG and IgA plaque-forming cells than AKR mice. In contrast, AKR mice produced T. spiralis-specific IgG2a, whereas the B10.BR mice did not. The antibody response kinetics of these strains were similar. We also analyzed lymphokine secretion after restimulating lymphocytes in vitro with T. spiralis Ag. The AKR mesenteric lymph node cells produced more IFN-gamma and less IL-4 than the B10.BR mesenteric lymph node cells. The B10.BR splenocytes produced more IL-4 than the AKR splenocytes, although splenocyte IFN-gamma production was not different. The kinetics of IL-4 production also differed between the two strains. In summary, resistant AKR mice produced more IFN-gamma and T. spiralis-specific IgG2a than susceptible B10.BR mice, which produced more IL-4, IgE, and T. spiralis-specific IgG1. Our results are consistent with differential activation of Th cell subsets in T. spiralis-infected AKR and B10.BR mice.</description><subject>Animals</subject><subject>Antibodies, Helminth - biosynthesis</subject><subject>Antibodies, Helminth - classification</subject><subject>Female</subject><subject>Immunity, Innate</subject><subject>Interferon-gamma - biosynthesis</subject><subject>Interleukin-4 - biosynthesis</subject><subject>Lymphocyte Activation</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred AKR</subject><subject>Rats</subject><subject>Rats, Inbred Strains</subject><subject>T-Lymphocytes, Helper-Inducer - immunology</subject><subject>T-Lymphocytes, Helper-Inducer - metabolism</subject><subject>Trichinella - growth &amp; development</subject><subject>Trichinella - immunology</subject><subject>Trichinella spiralis</subject><subject>Trichinellosis - immunology</subject><subject>Trichinellosis - parasitology</subject><issn>0022-1767</issn><issn>1550-6606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1989</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkclOwzAQhi0EKmV5A5B8QlxSvCVOjgiVRULiUs6WY49bIycpdkLF25PSgrhxmsO_aGY-hC4omQkiqps33zRD24UZFXxG2Uwwzg7QlOY5yYqCFIdoSghjGZWFPEYnKb0RQgrCxARNWM6plNUU1fMPb6E1gF0XsfXOQYS29zpg39rB9L5rcefwCsIaIl5gAyHgNNQJ-oTtEH27xIvozcq3o6JxWvuog09j3MF3_AwdOR0SnO_nKXq9ny_uHrPnl4enu9vnzAjK-izPWc0Yd7oYLwDroCgrWzBTcW1kzTUn3JZSu9wxEDU3peDCOsZKKakAKPkputr1rmP3PkDqVePTdl3dQjckJSsuCa2qf400F7SkcmsUO6OJXUoRnFpH3-j4qShRWwbqh4EaGSjK1JbBGLvc9w91A_Y3tH_6qF_v9JVfrjY-gkqNDmF0U7XZbP5WfQHRbZPS</recordid><startdate>19891215</startdate><enddate>19891215</enddate><creator>Pond, L</creator><creator>Wassom, DL</creator><creator>Hayes, CE</creator><general>Am Assoc Immnol</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>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>19891215</creationdate><title>Evidence for differential induction of helper T cell subsets during Trichinella spiralis infection</title><author>Pond, L ; Wassom, DL ; Hayes, CE</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c412t-552b223fa6155edfe689d62c93ac7b3a303d87af5f2e4b3c8434df2287714ee83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1989</creationdate><topic>Animals</topic><topic>Antibodies, Helminth - biosynthesis</topic><topic>Antibodies, Helminth - classification</topic><topic>Female</topic><topic>Immunity, Innate</topic><topic>Interferon-gamma - biosynthesis</topic><topic>Interleukin-4 - biosynthesis</topic><topic>Lymphocyte Activation</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred AKR</topic><topic>Rats</topic><topic>Rats, Inbred Strains</topic><topic>T-Lymphocytes, Helper-Inducer - immunology</topic><topic>T-Lymphocytes, Helper-Inducer - metabolism</topic><topic>Trichinella - growth &amp; development</topic><topic>Trichinella - immunology</topic><topic>Trichinella spiralis</topic><topic>Trichinellosis - immunology</topic><topic>Trichinellosis - parasitology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pond, L</creatorcontrib><creatorcontrib>Wassom, DL</creatorcontrib><creatorcontrib>Hayes, CE</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of immunology (1950)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pond, L</au><au>Wassom, DL</au><au>Hayes, CE</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Evidence for differential induction of helper T cell subsets during Trichinella spiralis infection</atitle><jtitle>The Journal of immunology (1950)</jtitle><addtitle>J Immunol</addtitle><date>1989-12-15</date><risdate>1989</risdate><volume>143</volume><issue>12</issue><spage>4232</spage><epage>4237</epage><pages>4232-4237</pages><issn>0022-1767</issn><eissn>1550-6606</eissn><abstract>The H-2-compatible mouse strains, AKR and B10.BR, exhibit disparate responses to infection with the parasitic nematode Trichinella spiralis. The resistant AKR mice expel intestinal adult worms faster than susceptible B10.BR mice. We tested antibody and lymphokine responses in these strains. With respect to antibody responses, the B10.BR mice had 3- to 10-fold more serum IgE and T. spiralis-specific IgG1 and IgA than AKR mice. The B10.BR mice also had greater numbers of IgG and IgA plaque-forming cells than AKR mice. In contrast, AKR mice produced T. spiralis-specific IgG2a, whereas the B10.BR mice did not. The antibody response kinetics of these strains were similar. We also analyzed lymphokine secretion after restimulating lymphocytes in vitro with T. spiralis Ag. The AKR mesenteric lymph node cells produced more IFN-gamma and less IL-4 than the B10.BR mesenteric lymph node cells. The B10.BR splenocytes produced more IL-4 than the AKR splenocytes, although splenocyte IFN-gamma production was not different. The kinetics of IL-4 production also differed between the two strains. In summary, resistant AKR mice produced more IFN-gamma and T. spiralis-specific IgG2a than susceptible B10.BR mice, which produced more IL-4, IgE, and T. spiralis-specific IgG1. Our results are consistent with differential activation of Th cell subsets in T. spiralis-infected AKR and B10.BR mice.</abstract><cop>United States</cop><pub>Am Assoc Immnol</pub><pmid>2531779</pmid><doi>10.4049/jimmunol.143.12.4232</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record>
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subjects Animals
Antibodies, Helminth - biosynthesis
Antibodies, Helminth - classification
Female
Immunity, Innate
Interferon-gamma - biosynthesis
Interleukin-4 - biosynthesis
Lymphocyte Activation
Male
Mice
Mice, Inbred AKR
Rats
Rats, Inbred Strains
T-Lymphocytes, Helper-Inducer - immunology
T-Lymphocytes, Helper-Inducer - metabolism
Trichinella - growth & development
Trichinella - immunology
Trichinella spiralis
Trichinellosis - immunology
Trichinellosis - parasitology
title Evidence for differential induction of helper T cell subsets during Trichinella spiralis infection
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