Human IgE-binding factors

Soluble CD23 (Fc epsilon RII) and interleukin 1 synergistically induce early human thymocyte maturation.

“…Subsequently, this molecule was shown to be identical to the low affinity receptor for IgE (Fcc-RII), which may also be expressed on monocytes/macrophages, eosinophiles, platelets, some T cells, and epidermal Langerhans cells (6). CD23 is a 45-kD membrane gly- Proliferative response after in vitro conditioning of thymic CD7+ precursors.…”

“…We have previously reported that enriched populations of B lymphocytes from blood produce factors (3,5) that promote in vitro development of blood-and bone marrow-derived CD7 + CD2 -precursors. Comparing the biochemical characteristics of this B cell-derived activity (3) to known B cell-derived molecules, we found its striking homology to soluble CD23 (sCD23 ; sFcERII) (6,7) . Using recombinant sCD23 (rsCD23) (7), we then assayed the effect of this molecule alone or with rIL-1 and/or rIL-2 on purified CD7 + thymic precursors .…”

Increased production of soluble CD23 in rheumatoid arthritis, and its regulation by interleukin‐4

“…This 45-kd transmembrane glycoprotein is also present on a variety of cell types, including T lymphocytes, monocytes (41, platelets (51, and eosinophils (6). By proteolytic cleavage of the extracellular domain of the CD23 antigen (7), these cells release several instable soluble forms and a stable 25-kd fragment (sCD23) (8). CD23 expression and sCD23 release are up-regulated by interleukin-4 (IL-4) (9-12) and Epstein-Barr virus (EBV) (13) but downregulated by glucocorticoids (14).…”

Fcε receptor II/CD23+ lymphocytes in atopic dermatitis. III. Aberrant control in thein vitroexpression of FcεRII/CD23 on peripheral blood T cells in atopic dermatitis

“…Low affinity Fc receptor for IgE (FCERII/CD23) is expressed on several haematopoietic cells including lymphocytes, monocytes/ macrophages, Langerhans cells (LC), platelets and eosinophils [1][2][3][4], It is reported that FCERII is involved in B cell growth and differentiation [5], regulates IgE synthesis by B cells [6][7][8], participates in parasite killing by eosinophils [9], and plays a role in antigen focusing on B cells and LC [10,11], Soluble products of FceRII, known as IgE-binding factor (BF), promote the proliferation of activated B cells and regulate IgE synthesis by IL-4-stimulated peripheral blood cells and B cells from atopic donors [12,13], Thus, FceRII functions in a variety of ways depending on the cell type that expresses it, FCERII expression is regulated by cytokines, IL-4 induces over-expression of FCERII on T and B cells, monocytes and LC, FCERII expression on T cells induced by mitogen and allergen is Correspondence: Masahiro Takigawa, MD, Department of Dermatology, Hamamatsu University School of Medicine, Hamamatsu 431-31, Japan, enhanced in the presence of IL-4 [14][15][16], On the other hand, interferon-gamma (IFN-y) inhibits the expression on IL-4-stimulated T and B cells [ 17,18], whereas monocytes and LC are stimulated to express FCERII by IFN-y [4,13,19], IFN-a suppresses FCERII expression on B cells, monocytes and LC [20], Patients with atopic dermatitis have various humoral and cell-mediated immune dysfunctions [21,22], We have shown that the proportion of FCERII+ lymphocytes in the peripheral blood correlates with the extent of atopic dermatitis, whereas such correlation is not observed in patients with eczematous dermatitis [23], FCERII+ lymphocytes from patients with extensive atopic dermatitis contain TE cells that preferentially express CD8, TE cells are detected among inflammatory cells of atopic dermatitis, and acute skin lesions are infiltrated by CD8+ T« cells [24], Therefore, a critical question is whether FCERII expression on T cells, especially on those with CD8, is intrinsic to atopic lymphocytes following stimulation or secondary to abnormal production of stimuli that induce FCERII,…”