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B‐lymphocyte depletion ameliorates Sjögren's syndrome in Id3 knockout mice
Author(s) -
Hayakawa Ikuko,
Tedder Thomas F.,
Zhuang Yuan
Publication year - 2007
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2007.02614.x
Subject(s) - knockout mouse , immunology , lymphocyte , lymphocyte subsets , biology , chemistry , immune system , cd8 , genetics , receptor
Summary Sjögren's syndrome is an autoimmune disease in which immune cells chronically attack the lachrymal and salivary glands. The Id3 knockout mouse is a newly established animal model for primary Sjögren's syndrome. To address the role of B cells in Sjögren's syndrome and autoimmune disease, we studied the effect of CD20 monoclonal antibody treatment on the disease in Id3 knockout mice. Antibody treatment at 2‐month intervals led to efficient and sustained B‐cell depletion in Id3 knockout mice. A significant improvement of histopathology was observed accompanied by the recovery of saliva secretory function after CD20 antibody treatment. We further show that serum immunoglobulin G3, which is abnormally high in untreated Id3 knockout mice, was reduced after CD20 antibody treatment. This study establishes a new animal model for immunotherapy of Sjögren's symptoms and suggests a possible link between immunoglobulin G3 and disease pathology in Id3 knockout mice.