Recent Progress in Immune Responses in Gut

Kawanishi, Hidenori

doi:10.1159/000171211

Cited by 8 publications

(6 citation statements)

References 23 publications

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“…In mice infected with hymenolepid tapeworms, BEFUS (1977) and ALGHALI (1987) demonstrated the appearance of antibody producing lymphocytes in the lamina propria of the small intestine, with a predominance of IgA containing cells. The rather uniform level of IgA antibodies seen along the length of the small intestine in the present study may be explained by the fact that IgA is produced locally in the intestinal wall, to a much higher degree than IgG and IgM (BEFUS & BIENENSTOCK, 1982;KAWANISHI, 1989).…”

Section: Discussionmentioning

confidence: 43%

The antibody response in serum, intestinal wall and intestinal lumen of NMRI mice infected with Echinostoma caproni

Agger¹,

Simonsen²,

Vennervald³

1993

J. Helminthol.

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Groups of mice (NMRI) were infected with 0.6 and 25 metacercariae of the intestinal trematode Echinostoma caproni. An enzyme linked immunosorbent assay (ELISA) was developed for measuring the specific IgM, IgG and IgA antibody responses in serum, small intestinal tissue and small intestinal lumen of the mice, by using a crude adult E. caproni antigen. In infected mice, significant levels of IgM were measured in the sera from day 14 after infection and of IgG and IgA from day 28 after infection. Early in the infection, the mean level of serum IgM was higher in 6-worm infections than in 25-worm infections. Late in the infection, higher mean levels of IgA were reached in the serum of mice with high than in those with low dose infections. The onset of appearance of antibodies in the tissue of the small intestine reflected the picture seen in the serum. For IgM, and to a lesser degree for IgG, the highest mean antibody levels appeared in the posterior sections of the small intestinal wall, where also the parasites were located. The mean level of IgA, however, was uniform throughout the length of the small intestinal tissue. High levels of specific IgA were detected in the lumen of the small intestine on day 28 after infection, especially in the anterior sections, where only few parasites were located. No specific IgM or IgG could be detected in the intestinal lumen on this day. The results are related to the intestinal location and the pattern of expulsion of E. caproni in the mouse host.

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Section: Discussionmentioning

confidence: 43%

The antibody response in serum, intestinal wall and intestinal lumen of NMRI mice infected with Echinostoma caproni

Agger¹,

Simonsen²,

Vennervald³

1993

J. Helminthol.

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“…In GALT, normal gut mucosal humoral immune responses are mainly under control by T cells, which include the C'D3+ CD4+ hclpcr/inducerT cell subset, CD3+ CD8' sup pressor T cell subset and putative CD3* CD4' class-specific immunoglobulin switch T cell subset [12] (fig. 2).…”

Section: Humoral Immunitymentioning

confidence: 99%

“…The oral mucosa is pro tected mostly by salivary IgA, whereas the dis tal gastrointestinal tract receives immuno globulin from either IgA-secreting plasma cells in lamina propria via enterocytes, or from hepatocytes or biliary duct epithelia via the hepatobiliary pathway [12,56] [6], Another study has reported a 2.5-fold decrease in IgA levels in supernatants collected from intestinal wash ings in fasting aged mice, as compared with those of middle-aged mice; in the nonfasting state, such as under cholinergic stimulation, aged lamina propria B cells are overreactive, with their maximal production of immuno globulin. particularly IgA.…”

Section: (D) Changes In Intestinal Intraluminalmentioning

confidence: 99%

“…The research that has been done on age-related alterations in gut mucosal immune processes is therefore limited [3][4][5][6][7][8][9]. In actual fact, the mucosal im mune system has unique features that can be distinguished from the rest of the lymphoid system [10][11][12][13][14][15][16], In addition, the mucosal im mune system plays a dual role in the lym phoid system: It mediates T cell-mediated im mune responses at gut mucosal sites ( fig. 1), and also in the entire body via the gastrointes tinal tract this 'entry' function affects the quality and quantity of the antigen-gaining access to the immune system as a whole.…”

Section: Introductionmentioning

confidence: 99%

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Recent Progress in Senescence-Associated Gut Mucosal Immunity

Kawanishi

1993

Dig Dis

Self Cite

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The immune response in gut-associated lymphoid tissues (GALT) is altered in the aging process. Senescence-induced quantitative decline and qualitative changes of GALT T and B cells and their subpopulations contribute largely to the impaired gut mucosal immune responses. Thus, not only direct cell-to-cell contact interactions, but also patterns of immuno-regulatory cytokine production and serum-soluble cytokine, such as interleukin-2 receptors are also altered, causing both cellular and humoral immune abnormalities in GALT. One of the characteristic features includes functional defects of suppressor T cells. As a consequence, relative hyperfunction of helper T cells ensues. The defective immune response of both function and control of aged GALT may help to explain the increased incidence of infection and neoplasia in the gastrointestinal tract with age. On the subcellular level, these aged T and B cells impair transmembranous signal transduction. Trials of immune interventions to reduce or reverse immunosenescence in GALT were made in animals. The results of adoptive transfer of in vitro educated helper T cells from aged GALT are encouraging. Further innovative immunologic interventions are indicated.

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“…Several recent studies have demonstrated that antigens are absorbed across the epithelium of the gut with the mature absorptive epithelial cells acting as modulators of immune responses [1,2]. Changes in epithelial cell surface glycoproteins and glycolipids have been linked to aberrant or accelerated cell growth, and expression of, and/or transformation of, antigenic epitopes on the cellular surface, particularly in malignant cells [3,4].…”

Section: Introductionmentioning

confidence: 99%

Expression of the 40 kD protein in DLD-1 colon cancer cells and the effect of cytokines

Das

Squillante

Robertson

1992

Clinical and Experimental Immunology

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SUMMARYWe recently reported the presence of an organ-specific 40 kD colonic protein which acts as an autoantigen(s) in patients with ulcerative colitis. Using a specific monoclonal antibody directed against 40 kD protein (7EI2H12, IgM isotype), in conjunction with immunocytochemistry and flow cytometry, we examined the presence of the 40 kD protein on human colon cancer cells, DLD-1, and also characterized the ability of cytokines, IFN-y and tumour necrosis factor, to modulate the expression of this protein on these tumour cells. The presence of the 40 kD protein was localized to the plasma membrane; less was present within the cytoplasm. Following exposure to IFN-y (10-1000 U/ ml), DLD-I colon tumour cells showed a dose-and time-dependent increase in 7E12H12 antibody associated immunofluorescence, with the maximum 7E12H12 antibody binding observed with 100 U/ml IFN-y at 48 h. In contrast, tumour necrosis factor did not alter the levels of anti-40 kD antibody binding over that of control cells. Since IFN-y is also known to induce class II major histocompatibility antigens, we examined the possibility of cross-reactivity of HLA class II antigens and Mr 40 kD epitope. Neither pre-incubation of DLD-I colon tumour cells with anti-HLA class II antibodies followed by 7E12H12 nor co-incubation of both antibodies altered the amount of 7E12H12 antibody binding. Using a direct ELISA, a highly enriched preparation of Mr 40 kD protein reactive to anti-40 kD antibody did not react with HLA class II antibodies. The present results suggest that 40 kD protein is present on DLD-1 human colon tumour cells and that although the 40 kD protein epitope expression is increased by the lymphocyte-derived cytokine, IFN-y, the epitope is separate and distinct from the class II HLA antigens. Further studies on the 40 KD protein may elucidate its autoantigenic role in the pathogenesis of inflammatory bowel disease.

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Recent Progress in Immune Responses in Gut

Cited by 8 publications

References 23 publications

The antibody response in serum, intestinal wall and intestinal lumen of NMRI mice infected with Echinostoma caproni

The antibody response in serum, intestinal wall and intestinal lumen of NMRI mice infected with Echinostoma caproni

Recent Progress in Senescence-Associated Gut Mucosal Immunity

Expression of the 40 kD protein in DLD-1 colon cancer cells and the effect of cytokines

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