Crohn's Disease Associated With Selective Immunoglobulin a Deficiency

Iizuka, Masahiro; Itou, Hiroaki; Sato, Michiko; Yukawa, Michihiro; Shirasaka, Tomoyuki; Chiba, Mitsuro; Watanabe, Sumio

doi:10.1111/j.1440-1746.2001.2379f.x

Cited by 6 publications

(7 citation statements)

References 3 publications

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“…Because the protective barrier of the gastrointestinal system is defective in SIgAD, protozoa such as Giardia lamblia can attach to the epithelium, proliferate and cause infection; however, mouse models have suggested that clearance is T cell‐mediated . As mentioned above, other gastrointestinal disorders reported in SIgAD patients include pernicious anaemia , Crohn's disease and ulcerative colitis .…”

Section: Clinical Manifestations In Patients With Sigadmentioning

confidence: 99%

Selective IgA Deficiency: Epidemiology, Pathogenesis, Clinical Phenotype, Diagnosis, Prognosis and Management

et al. 2017

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Selective immunoglobulin A deficiency (SIgAD) is the most common primary antibody deficiency. Although more patients with SIgAD are asymptomatic, selected patients suffer from different clinical complications such as pulmonary infections, allergies, autoimmune diseases, gastrointestinal disorders and malignancy. Pathogenesis of SIgAD is still unknown; however, a defective terminal differentiation of B cells and defect in switching to IgA-producing plasma cells are presumed to be responsible. Furthermore, some cytogenic defects and monogenic mutations are associated with SIgAD. There is no specific treatment for patients with symptomatic IgA deficiency, although prophylactic antibiotic therapy along with circumstantial immunoglobulin replacement with justification and supportive care (using a product that contains minimal IgA) could be helpful for patients with a severe phenotype. The epidemiology, pathogenesis, clinical phenotype, diagnosis, prognosis, management and treatment in patients with SIgAD have been reviewed.

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Section: Clinical Manifestations In Patients With Sigadmentioning

confidence: 99%

Selective IgA Deficiency: Epidemiology, Pathogenesis, Clinical Phenotype, Diagnosis, Prognosis and Management

et al. 2017

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“…Interestingly, it was reported that selective IgA deficiency is associated with some Th1 diseases, such as Crohn's disease (41), and with upregulated IL-12 production (42), although the latter could not be localized to monocytes. It also remains possible that the association between autoimmunity and IgA deficiency relates to a common genetic susceptibility (43).…”

Section: Inhibition Of Stat1 Activation By Igamentioning

confidence: 99%

FcαRI-Mediated Inhibition of IL-12 Production and Priming by IFN-γ of Human Monocytes and Dendritic Cells

Lecocq

Detry

Guisset

et al. 2013

The Journal of Immunology

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We showed that IgA induces IL-10 in monocytes and dendritic cells. Because reciprocal inhibition exists between IL-10 and IL-12, we explored whether IgA could regulate this other immunoregulatory cytokine. In human monocytes and monocyte-derived dendritic cells preincubated with IFN-γ before stimulation by LPS, suppression of p40 and IL-12p70 production was observed upon IgA treatment during IFN-γ priming. Washout experiments and inhibition of IFN-γ–induced CXCL10 (IP-10) and FcγRI (CD64) indicated that inhibition by IgA occurred at both the LPS and IFN-γ levels. Inhibition was not affected by blockade of IL-10 or MAPK but involved FcαRI/CD89-mediated suppression of STAT1 phosphorylation. These data indicate that FcαRI ligation on human monocytes and dendritic cells inhibits IL-12 expression and type 1 activation by interfering with STAT1 activation.

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“…The following GI manifestations have also been reported in isolated case reports in association with IgA deficiency: pernicious anemia 26,27 ; Crohn's disease (CD) and ulcerative colitis (UC) [28][29][30] ; lymphomas 24 ; and gastric carcinomas. 25 The actual prevalence of these diseases is not defined and whether these patients were purely IgA-deficient and not a variant of CVID is not known.…”

Section: Selective Iga Deficiencymentioning

confidence: 95%

Gastrointestinal manifestations in primary immune disorders

Agarwal

Mayer

2010

Inflammatory Bowel Diseases

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The gastrointestinal tract is the largest lymphoid organ in the body containing T and B lymphocytes, macrophages, and dendritic cells. Despite the fact that these cells are constantly confronted with antigen primarily in the form of food and bacteria, immune responses in the gut are tightly regulated to maintain homeostasis. Without this balance of active immunity and tolerance, mucosal inflammation may ensue, and manifest as Crohn's disease, ulcerative colitis, pernicious anemia, or celiac sprue. Therefore, it is not unreasonable that inflammatory diseases of the gut are commonly encountered in patients with primary immune deficiencies. The exact pathogenesis of gastrointestinal diseases in the setting of primary immunodeficiency remains unknown, however, both humoral and cell-mediated immunity appear to play a role in preventing intestinal inflammation. Patients presenting with atypical gastrointestinal disease and/or failure to respond to conventional therapy should be evaluated for an underlying primary immune disorder in order to initiate appropriate treatment, such as immunoglobulin or in more severe cases bone marrow transplantation, to prevent long term complications.

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Crohn's Disease Associated With Selective Immunoglobulin a Deficiency

Cited by 6 publications

References 3 publications

Selective IgA Deficiency: Epidemiology, Pathogenesis, Clinical Phenotype, Diagnosis, Prognosis and Management

Selective IgA Deficiency: Epidemiology, Pathogenesis, Clinical Phenotype, Diagnosis, Prognosis and Management

FcαRI-Mediated Inhibition of IL-12 Production and Priming by IFN-γ of Human Monocytes and Dendritic Cells

Gastrointestinal manifestations in primary immune disorders

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