Intestinal γ/δ Receptor-Bearing T Lymphocytes in Celiac Disease and Inflammatory Bowel Diseases in Children. Constant Increase in Celiac Disease

Savilahti, E; Arató, András; Verkasalo, M

doi:10.1203/00006450-199012000-00005

Cited by 125 publications

(88 citation statements)

References 12 publications

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“…Increased numbers of IgA-and IgM-secreting plasma cells in the lamina propria of the mucosa of CD patients compared with healthy children and the return to normal features with treatment are indicative of an immunity-associated disease (34). Similarly, the intraepithelial infiltration of CD8+ T lymphocytes and the increased proportion of CD3+ T cells expressing the y16-receptor in CD patients suggest that the tissue damage occurs as a consequence of the immune response (35,36).…”

Section: Resultsmentioning

confidence: 96%

Reactivity of Gliadin and Lectins with Celiac Intestinal Mucosa1

Pittschieler¹,

Ladinser²,

Petell³

1994

Pediatr Res

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The binding patterns of gliadin and selected lectins to jejunal biopsy specimens obtained from children with total villous atrophy during active celiac disease (CD; 19 patients) and in remission (16 patients) were examined by light microscopy. Three categories of carbohydratespecific lectins were chosen for the study: those recognizing mannose/glucose residues, those recognizing N-acetylglucosamine/glucose (glcNAc/glc) residues, and those recognizing N-acetylgalactosamine/galactose (galNAc/gal) residues. The galNAc/gal lectins, with the exception of phaseolus vulgaris agglutinin variants, presented a typical staining of the luminal surface of the jejunal mucosa obtained from CD patients. However, these lectins displayed no reactivity to jejunal sections of CD patients in remission or control biopsies that included healthy children (25 children) and patients suffering from cow milk protein allergy (10 children). The glcNAc/glc lectin showed a strong preferential recognition of CD jejunal tissue but also bound with less intensity to specimens from patients with cow milk allergies and healthy children. Unlike other galNAc/ gal lectins, phaseolus vulgaris agglutinin variants were indistinguishable in their binding patterns to the mucosa of control groups and CD patients in remission and failed to react to CD biopsies. The mannose/glc lectins were not distinctive in their binding patterns. In all cases, lectin binding was specifically inhibited by the lectins' competitive saccharides. Atypical of lectin binding patterns, gliadin reactivity was restricted to intracellular areas of enterocytes and was unique to active CD mucosa. The pathogenesis of childhood and adult CD is still not well understood (1, 2). CD in childhood is characterized by villous atrophy and an increase in both the number of damaged enterocytes and the cell turnover (3). The precise mechanisms responsible for these changes are still

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Section: Resultsmentioning

confidence: 96%

Reactivity of Gliadin and Lectins with Celiac Intestinal Mucosa1

Pittschieler¹,

Ladinser²,

Petell³

1994

Pediatr Res

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“…Increased numbers and an increased proportion of / relative to / IEL in the small intestinal mucosa are a hallmark of coeliac disease, whether disease is active or in remission [15][16][17]. In addition, healthy first degree relatives of coeliac disease patients have increased numbers of / IEL in the small intestinal mucosa, and this correlates with whether or not those subjects express the HLA class II coeliac disease susceptibility alleles [20].…”

Section: Discussionmentioning

confidence: 99%

“…In contrast, T cells that express the / form of the TCR are abundant in the lamina propria and intraepithelial region. In addition to active coeliac disease, patients with treated coeliac disease are reported to have an increased proportion of / IEL to / IEL, and this finding has been used as a diagnostic adjunct for latent coeliac disease [15][16][17][18][19]. Furthermore, increased numbers of mucosal / T cells have been noted in otherwise healthy, first degree relatives of coeliac disease patients who carry the disease-associated HLA class II susceptibility alleles [20].…”

Section: Introductionmentioning

confidence: 99%

“…Furthermore, increased numbers of mucosal / T cells have been noted in otherwise healthy, first degree relatives of coeliac disease patients who carry the disease-associated HLA class II susceptibility alleles [20]. Increased numbers of / T cells in the intestinal mucosa do not appear to simply reflect mucosal inflammation, since / T cells are rarely increased in other chronic inflammatory mucosal states, such as tropical sprue, inflammatory bowel disease, or during microbial infection of the intestinal tract [10,15,21].…”

Section: Introductionmentioning

confidence: 99%

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Distinct δ T cell receptor repertoires in monozygotic twins concordant for coeliac disease

Holtmeier

Rowell

Nyberg

et al. 1997

Clinical and Experimental Immunology

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SUMMARYOne of the hallmarks of coeliac disease, both active and treated, is an increased number and proportion of°/± intraepithelial T lymphocytes in the small intestinal mucosa, and an increased number of°/± T cells in the small intestinal mucosa of coeliac disease patients has been associated with the inheritance of specific HLA class II DQ alleles. Nonetheless, the contribution of genetic factors to the development of the T cell receptor (TCR) ± repertoire in coeliac disease is not known. We have assessed the contribution of genetic factors to development of the TCR ± repertoire in coeliac disease, by characterizing the junctional diversity of TCR ± transcripts expressed in the intestine and peripheral blood of a pair of monozygotic (MZ) twins concordant for coeliac disease. TCR V±1, V±2 and V±3 transcripts from small intestinal and colon biopsies, and from peripheral blood mononuclear cells, were amplified by polymerase chain reaction (PCR) and the complementarity determining region (CDR)3 domains of TCR ± transcripts were analysed by denaturing PAGE and direct nucleotide sequencing. The repertoire of TCR ± transcripts and CDR3 amino acid motifs in the intestine and peripheral blood of MZ twins concordant for coeliac disease exhibited no overlap. The TCR ± repertoire in each twin was oligoclonal, and complexity of the junctional regions of their TCR ± transcripts was typical of the repertoire in healthy adults. Thus, genetically identical individuals with coeliac disease have distinct, non-overlapping TCR ± repertoires. Moreover, genetic factors that determine disease susceptibility do not appear to select for specific TCR ± sequences or CDR3 amino acid motifs. Keywords ±T cell receptor coeliac disease monozygotic twins T cell receptor repertoire°/

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“…These include a flat mucosal surface, absence of villi, crypt hyperplasia, and extensive infiltration of the lamina propria by lymphocytes [1,2]. Previous studies have demonstrated that the proportion of T cells bearing the 8f J cell receptor {6'y T cells) is increased in the jejunum of patients with active [3,4], treated [5] and latent [6] coeliac disease.…”

Section: Introductionmentioning

confidence: 99%

Predominance of T cell receptor Vδ3 in small bowel biopsies from celiac disease patients

Falk

Zhang

et al. 1994

Clinical and Experimental Immunology

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SUMMARYIncreased numbers of T cells bearing the 7^ antigen receptor {•^8 T cells) have been reported in small bowel biopsies of patients with latent, active or treated coeliac disease. We have studied jejunal biopsies from seven children with coeliac disease and 10 children with normal gut histology to characterize 7* T cell receptor (TCR) variable region gene subfamily expression in resident 7* T cells and compared the results with the findings in peripheral blood mononuclear cells (PBMC) obtained on the same day as the gut biopsy. Molecular analysis of RNA extracted from PBMC and biopsies was performed by reverse transcription and amplification with the polymerase chain reaction using primers specific for six TCR V5 families and four TCR V7 families. We report, first, that a significantly increased number of 7* T cells expressing the TCR V53 subfamily {P = 0008) was observed in jejunal biopsies from children with coeliac disease, and second, that 75 T cell V region subfamily populations in gut differed from those seen in PBMC for both control and coeliac patients. Significantly reduced numbers of TCR V62, V(53, V65 {P < 0 01) and V72, V7^4 {P < 0 01) T cells were found in gut compared with PBMC. The difference in 7^ T cell repertoire observed between gut and blood may reflect differences in the nature of the antigens usually encountered in these two compartments. The over-representation of TCR V(53 in patients with coeliac disease suggests a specific role for these cells in the induction or maintenance of the jejunal abnormality associated with this disease.

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Intestinal γ/δ Receptor-Bearing T Lymphocytes in Celiac Disease and Inflammatory Bowel Diseases in Children. Constant Increase in Celiac Disease

Cited by 125 publications

References 12 publications

Reactivity of Gliadin and Lectins with Celiac Intestinal Mucosa1

Reactivity of Gliadin and Lectins with Celiac Intestinal Mucosa1

Distinct δ T cell receptor repertoires in monozygotic twins concordant for coeliac disease

Predominance of T cell receptor Vδ3 in small bowel biopsies from celiac disease patients

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