Expression and role of CR1 and CR2 on B and T lymphocytes under physiological and autoimmune conditions

Erdei, Anna; Isaák, Andrea; Török, Katalin; Sándor, Noémi; Kremlitzka, Mariann; Prechl, József; Bajtay, Zsuzsa

doi:10.1016/j.molimm.2009.05.181

Cited by 74 publications

(55 citation statements)

References 79 publications

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“…Furthermore, even if the CLU and CR1 genes are not annotated in the KEGG immune response pathways we picked-up, this hypothesis would be in accordance to our initial results in- volving CLU and CR1 as major genetic determinants of AD in influencing susceptibility to late onset forms of the disease through a role in Aβ clearance [3]. Furthermore it is worth noting that CR1 might act as either activator or inhibitor of B cell and T cell functions [33]. Interestingly CR1 is mainly expressed in the choroid plexus in the brain [34] and the choroid plexus could represent a site for lymphocyte entry in the CSF and brain, and for presentation of antigens [35].…”

Section: Discussionsupporting

confidence: 65%

Implication of the Immune System in Alzheimer's Disease: Evidence from Genome-Wide Pathway Analysis

Lambert

Grenier‐Boley

Chouraki

et al. 2010

JAD

133

119

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Abstract. The results of several genome-wide association studies (GWASs) in the field of Alzheimer's disease (AD) have recently been published. Although these studies reported in detail on single-nucleotide polymorphisms (SNPs) and the neighboring genes with the strongest evidence of association with AD, little attention was paid to the rest of the genome. However, complementary statistical and bio-informatics approaches now enable the extraction of pertinent information from other SNPs and/or genes which are only nominally associated with the disease risk. Two different tools (the ALIGATOR and GenGen/KEGG software packages) were used to analyze a large GWAS dataset containing 2,032 AD cases and 5,328 controls. Convergent outputs from the two gene set enrichment approaches suggested an immune system dysfunction in AD. Furthermore, although these statistical approaches did not adopt a priori hypotheses concerning a biological function's putative role in the disease process, genes associated with AD risk were overrepresented in the "Alzheimer's disease" KEGG pathway. In conclusion, a systematic search for biological pathways using GWAS data set seems to comfort the primary causes already suspected but may specifically highlight the importance of the immune system in AD.

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Section: Discussionsupporting

confidence: 65%

Implication of the Immune System in Alzheimer's Disease: Evidence from Genome-Wide Pathway Analysis

Lambert

Grenier‐Boley

Chouraki

et al. 2010

JAD

133

119

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“…However, T cells have been reported to express CR2, the cognate receptor for C3d (14)(15)(16)(17). We therefore wondered whether C3d might govern immune surveillance by interacting with CR2.…”

Section: Resultsmentioning

confidence: 99%

C3d regulates immune checkpoint blockade and enhances antitumor immunity

Platt¹,

Silva

Balin

et al. 2017

JCI Insight

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“…SLE, RA) [62]. Another important function of the C system is the modulation of B-and T-cell responses through interactions of C1q and C3 opsonized particles and (apoptotic) cells with C receptors on these cells and on dendritic cells (for reviews see [58,63,64]. …”

Section: Functions Of Complementmentioning

confidence: 99%

Histological and Direct Evidence for the Role of Complement in the Neuroinflammation of AD

Veerhuis

2011

CAR

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In Alzheimers's disease (AD) a disturbed balance between synthesis and removal of Aβ leads to the formation of Aβ deposits and a reaction of the innate immune system. Little evidence exists for a contribution of the adaptive immune response in AD, as no signs of influx of blood borne cells or presence of immunoglobulins in Aβ deposits are apparent. Factors of the complement(C) system and pentraxins act as pattern recognition molecules and mediate uptake of Aβ by glial cells expressing C-receptors (Crec). These interactions may, however, also lead to synthesis and secretion of reactive oxygen species (ROS), cytokines, chemokines and other potentially neurotoxic agents by the glial cells. Virtually all complement factors are produced in brain, and the expression is increased in AD affected brain areas. In AD brain areas with amyloid deposits especially classical pathway C activation products are readily observed. Also C regulatory proteins (Creg) and Crec can be found in the brain parenchyma and are upregulated, especially under acute inflammatory conditions, such as meningitis. However, under chronic low-grade inflammatory conditions, such as in AD, Creg and to some extent Crec expression may remain at a low level, thereby allowing C activation to proceed, leading to sustained activation of glial cells and neurodegenerative changes. In this review evidence from immunohistochemical, in vitro and animal studies pointing to a role for C activation is discussed, with special focus on the disturbed balance between C activators and Cregs in AD.

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Expression and role of CR1 and CR2 on B and T lymphocytes under physiological and autoimmune conditions

Cited by 74 publications

References 79 publications

Implication of the Immune System in Alzheimer's Disease: Evidence from Genome-Wide Pathway Analysis

Implication of the Immune System in Alzheimer's Disease: Evidence from Genome-Wide Pathway Analysis

C3d regulates immune checkpoint blockade and enhances antitumor immunity

Histological and Direct Evidence for the Role of Complement in the Neuroinflammation of AD

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