Excess IL-12 but not IL-23 Accompanies the Inflammatory Bowel Disease Associated With Common Variable Immunodeficiency

Mannon, Peter J.; Fuss, Ivan J.; Dill, Susie; Friend, Judith; Groden, Catherine; Hornung, Ron; Yang, Zhaopeng; Yi, Chuli; Quezado, Martha; Brown, Margaret R.; Strober, Warren

doi:10.1053/j.gastro.2006.06.022

Cited by 100 publications

(78 citation statements)

References 51 publications

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“…CVID patients with hepatomegaly had higher IL-2 and IFN-γ levels in stimulated CD4 + T cells, and patients with granuloma were found to have higher CCR5 expression in CD4 + T cells, suggesting that T H 1 cells may play a role in granuloma formation in CVID patients [14]. Overall, increased production of some chemokines [56] and cytokines, including IFN-γ [57], TNF-α [12], IL-12 [57], IL-9 [49], IL-4, and IL-10 [58] by T H subsets has been reported in CVID patients [59]. Some of these cytokines play a pivotal role in antibody synthesis.…”

Section: Helper T-cell Defectsmentioning

confidence: 96%

T-Cell Abnormalities in Common Variable Immunodeficiency

Azizi

Rezaei

Kiaee

et al. 2016

J Investig Allergol Clin Immunol

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Common variable immunodeficiency (CVID) is the most common clinical primary immunodeficiency. It is characterized by a defect in B-cell differentiation to plasma and memory B cells. Moreover, numerous T-cell abnormalities have been reported and include decreased T-cell count and proliferative response, increased T-cell activation and apoptosis, and abnormalities in cytokine production. The aims of this review are to describe phenotypic and functional defects in T cells in CVID patients and to review the literature with respect to the effects of immunoglobulin replacement on the T-cell component in CVID patients. Key words: Common variable immunodeficiency. T cell. Helper T cells. Regulatory T cells. ResumenLa inmunodeficiencia común variable (CVID) es la inmunodeficiencia primaria más frecuente. Se caracteriza por un defecto en la diferenciación de linfocitos B hacia células plasmáticas y linfocitos B memoria. Se han descrito numerosas alteraciones en los linfocitos T de estos pacientes, tales como disminución en el número de linfocitos T y en sus respuestas proliferativas, aumento en la activación de células T y en la apoptosis, así como alteraciones en la producción de citokinas. El objetivo de esta revisión es describir las alteraciones funcionales y fenotípicas de los linfocitos T en los pacientes con CVID y revisar la bibliografía en relación a los efectos que la administración de inmunoglobulinas produce en los linfocitos T de los pacientes con CVID. Palabras clave: Inmunodeficiencia común variable. Células T. Células T helper. Células T reguladoras.

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Section: Helper T-cell Defectsmentioning

confidence: 96%

T-Cell Abnormalities in Common Variable Immunodeficiency

Azizi

Rezaei

Kiaee

et al. 2016

J Investig Allergol Clin Immunol

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“…Unlike classical IBD, lamina propria lymphocytes from CVID patients with large bowel enteropathy are skewed toward the production of Th1 proinflammatory cytokines, such as interleukin-12 (IL-12) and gamma interferon (IFN-) rather than TNF-alpha, IL17, or IL23, suggesting that the pathogenesis of the lesions differs at least partially (21). CVID-associated enteropathy may be suspected on the basis of the lack of plasma cells in a GI biopsy, but because this feature is only present in about two-thirds of patients, the diagnosis cannot always be confirmed in the absence of other clinical and laboratory findings (22).…”

Section: Cvid and Inflammationmentioning

confidence: 99%

Common variable immunodeficiency: Crossroads between infections, inflammation and autoimmunity

Baldovino

Montin

Martino

et al. 2013

Autoimmunity Reviews

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“…First, IVIg therapy only substitutes IgG, whilst IgA (the major secretory antibody at mucosal surfaces) is not replaced. Other possible explanations could be ongoing inflammation after treated infections [75] and concurrent T-cell defects [3,75].…”

Section: Benefit In Gastrointestinal Diseasementioning

confidence: 99%

Immunoglobulin treatment in primary antibody deficiency

Maarschalk-Ellerbroek

Hoepelman

Ellerbroek

2011

International Journal of Antimicrobial Agents

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The primary antibody deficiency syndromes are characterised by recurrent respiratory tract infections and the inability to produce effective immunoglobulin (Ig) responses. The best known primary antibody deficiencies are common variable immunodeficiency (CVID), X-linked agammaglobulinaemia (XLA), immunoglobulin G (IgG) subclass deficiency, and selective antibody deficiency with normal immunoglobulins (SADNI).Therapy in these patients consists of prophylactic antibiotics and/or Ig replacement therapy. Diagnostic delay remains common owing to limited awareness of the presenting features and may result in increased morbidity and mortality. Replacement therapy with immunoglobulins increases life expectancy and reduces the frequency and severity of infections, but the effect on end-organ damage is still unknown. Both intravenous immunoglobulin (IVIg) and subcutaneous immunoglobulin (SCIg) treatment appear to be safe, with comparable efficacy. A starting dose of 300-400 mg/kg/month in IVIg and 100 mg/week for SCIg is recommended. IgG trough levels should be >5 g/L for patients with agammaglobulinaemia and 3 g/L greater than the initial IgG level for patients with CVID; however, the clinical response should be foremost in choosing the dose and trough level. Infusion-related adverse reactions are generally mild owing to improved manufacturing processes. In this paper, aspects of Ig replacement therapy in primary antibody-deficient patients will be addressed.

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Excess IL-12 but not IL-23 Accompanies the Inflammatory Bowel Disease Associated With Common Variable Immunodeficiency

Cited by 100 publications

References 51 publications

T-Cell Abnormalities in Common Variable Immunodeficiency

T-Cell Abnormalities in Common Variable Immunodeficiency

Common variable immunodeficiency: Crossroads between infections, inflammation and autoimmunity

Immunoglobulin treatment in primary antibody deficiency

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