PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 5932772

Immunogenesis, leukemogenesis and experimental auto-immunity.

R D Good·A E Gabrielsen·M D Cooper·R A Peterson·J Finstad
View original source ↗Export metadata ↓

Abstract

The source did not provide an abstract. Follow the original record for more information.

Explore related subjects

AgammaglobulinemiaAnimalsAutoimmune DiseasesHumansLymphoid TissueLymphomaMiceRabbitsRatsJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

R D Good, A E Gabrielsen, M D Cooper, R A Peterson, J Finstad. 1966. Immunogenesis, leukemogenesis and experimental auto-immunity.. https://pubmed.ncbi.nlm.nih.gov/5932772/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2006

Impaired Toll-like receptor 8-mediated IL-6 and TNF-alpha production in antigen-presenting cells from patients with X-linked agammaglobulinemia.

The critical role of Bruton tyrosine kinase (Btk) in B cells has been documented by the block of B-cell development in X-linked agammaglobulinemia (XLA). Less is known about Btk function in myeloid cells. Several pieces of evidence indicate that Btk is a component of Toll-like receptor (TLR) signaling. We analyzed whether Btk deficiency in XLA is associated with an impaired dendritic cell (DC) compartment or defective TLR signaling. We analyzed the expression of TLRs 1 to 9 on myeloid DCs generated from XLA patients and evaluated their response to activation by specific TLR agonists. We show that XLA patients have normal numbers of circulating DCs. Btk-deficient DCs have no defect in response to stimulation of TLRs 1/2, 2/6, 3, 4, and 5 but display a profound impairment of IL-6 and TNF-alpha production in response to stimulation by TLR-8 cognate agonist, ssRNA. These findings may provide an explanation for the susceptibility to enteroviral infections in XLA patients.

Agammaglobulinemia↗