Mast Cells, Tissue Histamine and Eosinophils in Early- and Late-Phase Skin Reactions: Effects of a Single Dose of Prednisolone

1990 ◽  
Vol 93 (2-3) ◽  
pp. 171-177 ◽  
Author(s):  
Ann Hammarlund ◽  
Ulf Pipkorn ◽  
Lennart Enerbäck
Keyword(s):  
Single Dose ◽  
Mast Cells ◽  
Late Phase ◽  
Skin Reactions ◽  
Tissue Histamine

IL-4– and IL-5–positive T lymphocytes, eosinophils, and mast cells in allergen-induced late-phase cutaneous reactions in atopic subjects☆☆☆★★★

1998 ◽  
Vol 101 (2) ◽  
pp. 222-230 ◽  
Author(s):  
Luis T. Barata ◽  
Sun Ying ◽  
Qiu Meng ◽  
Julia Barkans ◽  
Karalasingam Rajakulasingam ◽  
...  
Keyword(s):  
Mast Cells ◽  
T Lymphocytes ◽  
Late Phase ◽  
Cutaneous Reactions

Prednisolone Inhibits an IgE-Mediated Late-Phase Allergic Cutaneous Reactionby Interfering w ith the Activation of Mast Cells in Mice

Pharmacology ◽  
2001 ◽  
Vol 62 (1) ◽  
pp. 17-22 ◽  
Author(s):  
Masahiro Kimata ◽  
Toru Abe ◽  
Itaru Yamaguchi ◽  
Kanako Mito ◽  
Masako Tsunematsu ◽  
...  
Keyword(s):  
Mast Cells ◽  
Late Phase ◽  
Ige Mediated

scholarly journals Involvement of Bruton's Tyrosine Kinase in FcεRI-dependent Mast Cell Degranulation and Cytokine Production

1998 ◽  
Vol 187 (8) ◽  
pp. 1235-1247 ◽  
Author(s):  
Daisuke Hata ◽  
Yuko Kawakami ◽  
Naoki Inagaki ◽  
Chris S. Lantz ◽  
Toshio Kitamura ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Tyrosine Kinase ◽  
Bone Marrow Cells ◽  
Late Phase ◽  
Cell Development ◽  
Mutant Mice ◽  
Bruton’S Tyrosine Kinase ◽  
Bruton's Tyrosine Kinase ◽  
Retroviral Transfer

We investigated the role of Bruton's tyrosine kinase (Btk) in FcεRI-dependent activation of mouse mast cells, using xid and btk null mutant mice. Unlike B cell development, mast cell development is apparently normal in these btk mutant mice. However, mast cells derived from these mice exhibited significant abnormalities in FcεRI-dependent function. xid mice primed with anti-dinitrophenyl monoclonal IgE antibody exhibited mildly diminished early-phase and severely blunted late-phase anaphylactic reactions in response to antigen challenge in vivo. Consistent with this finding, cultured mast cells derived from the bone marrow cells of xid or btk null mice exhibited mild impairments in degranulation, and more profound defects in the production of several cytokines, upon FcεRI cross-linking. Moreover, the transcriptional activities of these cytokine genes were severely reduced in FcεRI-stimulated btk mutant mast cells. The specificity of these effects of btk mutations was confirmed by the improvement in the ability of btk mutant mast cells to degranulate and to secrete cytokines after the retroviral transfer of wild-type btk cDNA, but not of vector or kinase-dead btk cDNA. Retroviral transfer of Emt (= Itk/Tsk), Btk's closest relative, also partially improved the ability of btk mutant mast cells to secrete mediators. Taken together, these results demonstrate an important role for Btk in the full expression of FcεRI signal transduction in mast cells.

scholarly journals Lyn Is Essential for Fcγ Receptor III–Mediated Systemic Anaphylaxis but Not for the Arthus Reaction

2001 ◽  
Vol 193 (5) ◽  
pp. 563-572 ◽  
Author(s):  
Takae Yuasa ◽  
Masao Ono ◽  
Takeshi Watanabe ◽  
Toshiyuki Takai
Keyword(s):  
Mast Cells ◽  
Therapeutic Potential ◽  
Late Phase ◽  
Interleukin 4 ◽  
Arthus Reaction ◽  
Selective Treatment ◽  
Systemic Anaphylaxis ◽  
Inhibitory Signaling

The Src family kinase Lyn initiates intracellular signal transduction by associating with a variety of immune receptors such as antigen receptor on B cells and high-affinity Fc receptor (FcR) for immunoglobulin Ig(E) (FcεRI) on mast cells. Involvement of Lyn in the IgE-mediated immediate-type hypersensitivity is well documented, but the physiological significance of Lyn in IgG-dependent, type III low-affinity FcR for IgG (FcγRIII)-mediated responses is largely unknown. In this study, we generated a double-mutant mouse strain deficient in both type II FcR for IgG (FcγRIIB) and Lyn to exclude any involvement of inhibitory signaling by FcγRIIB, which otherwise downregulates FcγRIII-mediated cellular responses. FcγRIIB-deficient but Lyn-sufficient mice served as controls. The Lyn deficiency attenuated IgG-mediated systemic anaphylaxis in vivo, and significantly reduced calcium mobilization and degranulation responses of bone marrow–derived mast cells (BMMCs) in vitro. However, we found that either interleukin 4 or tumor necrosis factor α release by BMMCs was comparable to that from Lyn-deficient and control mice, and the reverse-passive Arthus reaction was equally induced in both mutant mice, indicating that Lyn is not involved in the onset of the IgG-mediated, FcγRIII-dependent late phase responses of mast cells. These findings provide us with insight into distinct signaling mechanisms in mast cells underlying the development of diverse pathologies as well as a therapeutic potential for selective treatment of allergic disorders.

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