Acquired but reversible loss of erythrocyte complement receptor 1 (CR1, CD35) and its longitudinal alteration in patients with severe acute respiratory syndrome

Abstract

This longitudinal study investigates the change of erythrocyte complement receptor (E-CR1) expression in patients with severe acute respiratory syndrome (SARS). Circulating E-CR1 expression was semiquantified by flow cytometric analyses in 54 SARS patients and in 212 healthy individuals as a control. Since E-CR1 expression is influenced by the genetic polymorphisms in the CR1 gene, a major genetic polymorphism located within intron 27 of the CR1 gene was simultaneously analysed by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). The results showed that the expression level of E-CR1 (referred to as net fluorescence intensity values, NFI) was statistically correlated with the relevant genetic genotypes among the Chinese population including the healthy individuals (NFI: 5.14 +/- 0.82, 3.57 +/- 0.66 and 2.67 +/- 0.32 for HH, HL and LL genotypes, respectively) and SARS patients (NFI: 3.52 +/- 0.91 and 2.63 +/- 0.70 for HH and HL genotypes, respectively). Interestingly, the expression density of E-CR1 was found to fall significantly during the initiation and progressive phases (weeks 1 and 2 after the disease onset) and gradually returned close to normal through their whole convalescent phase (beginning from weeks 2 or 3 to weeks 7 or 8) in SARS patients irrespective CR1 genotype. In conclusion, our findings, at least, suggest that E-CR1 is likely involved in immune pathogenesis of SARS disease.

Longitudinal alteration of circulating dendritic cell subsets and its correlation with steroid treatment in patients with severe acute respiratory syndrome

“…Previous reports suggested that SARS-CoV infection probably induced mild immunosuppression, and that immune function was further suppressed by high-dose steroid treatment [26,28]. However, it is still unclear how the human immune system is impaired in SARS infection.…”

Complement Receptor 1: Disease associations and therapeutic implications

“…In Leishmanial infections the CR1 receptor has been shown to be involved in the binding of Leishamania major metacyclic promastigotes to human macrophages (Da Silva et al, 1989;Rosenthal et al, 1996). The levels of E-CR1 decline during phases of initiation and progression of severe acute respiratory syndrome (SARS) (Wang et al, 2005). The expression of CR1 on the neutrophils of patients with severe atopic dermatitis was higher than those with the mild form of the disease (Yoshida et al, 2002).…”

Complement Receptor 1 and 2 Deficiency Increases Coxsackievirus B3-Induced Myocarditis, Dilated Cardiomyopathy, and Heart Failure by Increasing Macrophages, IL-1β, and Immune Complex Deposition in the Heart

“…CR1 levels are significantly lower in SLE patients, and genetically susceptible CR1/2-deficient mice develop increased lupus-like disease (5,9,10,54). Molecular genetics studies and analysis of twin pairs discordant for the presence of SLE suggest that reduced levels of CR1 are an acquired phenomenon (55,56). Thus, it is possible that viral or bacterial infections could reduce CR1 expression resulting in increased autoimmune disease in susceptible individuals.…”