The immunology of gluten hypersensitivity and celiac disease has been pursued with significant interest in the past 20 years. For the prevention of systemic diseases, most pathogens that gain entry into our bodies must be met with an effective immune response, yet in the gastrointestinal tract it is equally important that commensal bacteria and a diverse collection of dietary proteins and peptides be recognized without eliciting an active immune response or constant activation of the inflammatory pathway. This phenomenon of hyporesponsiveness to food antigens is known as oral tolerance. This oral tolerance to dietary antigens is maintained by three different mechanisms: anergy, cell deletion and immune suppression. However, in the presence of mechanical/chemical stressors and infections, this tolerance may break down, and gut associated lymphoid tissues (GALT) will react to different luminal antigens. The reaction of GALT to these antigens may lead to the production of pro-inflammatory cytokines, opening of tight junctions, entry of undigested antigens into the circulation, and the subsequent production of IgA, IgG, IgM and IgE antibodies in blood and secretory components. Like any other food hypersensitivity reaction, gluten sensitivity can be divided into immediate and delayed hypersensitivities. In this review an attempt is made first to differentiate immediate hypersensitivity to gliadin, mediated by IgE, from delayed hypersensitivity, which is mediated by IgA and IgG. Furthermore, we attempt to differentiate between gluten hypersensitivity with enteropathy (celiac disease) and gluten hypersensitivity without enteropathy.

ObjectivesIndividuals with HIV infection often have early waning of protective antibody following hepatitis B virus (HBV) vaccination. HIV viraemia at the time of vaccination may limit the durability of serum anti-HBV surface antibody (HBsAb) levels. We investigated the relationship of HIV plasma viral load (VL) and duration of HBsAb among vaccinees enrolled in the US Military HIV Natural History Study. MethodsWe included in the study participants who had no history of prior HBV infection, who had received all HBV vaccine doses after HIV diagnosis, and who had demonstrated an initial vaccine response, defined as HBsAb ≥ 10 IU/L. Responders were retrospectively followed with serial HBV serology from the time of the last vaccine dose until the development of waning (HBsAb < 10 IU/L) or the last HBsAb measurement. Time to and risk for waning were evaluated with Kaplan−Meier survival methods and Cox proportional hazards models, respectively. ResultsA total of 186 initial vaccine responders were identified. During 570 person-years of observation, HBsAb waned in 52 of 186 participants (28%). The cumulative proportion maintaining HBsAb ≥ 10 IU/L was 83% at 2 years and 56% at 5 years. Participants with an undetectable VL [hazard ratio (HR) 0.37; 95% confidence interval (CI) 0.18-0.76] or with detectable VL of ≤ 10 000 copies/mL (HR 0.46; 95% CI 0.21-1.00) had reduced risk of waning. Other factors including age, number of vaccine doses, CD4 count, and receipt of highly active antiretroviral therapy (HAART) were not significantly associated with risk of waning HBsAb. ConclusionsUndetectable or low HIV VL at the time of HBV vaccination is associated with greater durability of vaccine response in patients with HIV infection.

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Exposure to certain environmental factors during childhood may influence the developing immune system, causing predisposing or protective effects toward development of autoimmune disorders. This study examines the hypothesis that past infection with parvovirus B19, a common childhood infection, is associated with altered levels of subclinical inflammatory activity in presumably healthy adults. Qualitative anti-parvovirus B19 IgG antibody and high-sensitivity C-reactive protein were determined in serum samples from adult blood bank donors. C-reactive protein values of B19 IgG-positive and B19 IgG-negative groups were compared. Analysis was performed on 282 blood bank donor serum samples. Among donors aged 17-49 years (n = 152), B19 IgG-positive samples (57.9%) were associated with significantly lower C-reactive protein levels compared with B19 IgG-negative samples (median C-reactive protein: 1.30 mg/l vs. 2.65 mg/l; p = 0.012 unadjusted (Mann-Whitney U-test); p = 0.014 adjusted for gender and age (logistic regression)). Among donors aged >49 years, median C-reactive protein levels were identical by B19 IgG status. The association of B19 IgG antibody with lower C-reactive protein levels in the serum of younger adults supports the hypothesis that infection in childhood may contribute long-term beneficial adaptive immune responses.