Receptor for antibodies

Lisowska and Duk (1975a,b) have recently presented evidence suggesting that, although antigenic activity may indeed be dependent upon the sialic-acid-containing carbohydrate chains, differences in specificity between the M and N activities may reside in genetically controlled peptide sequences. 

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These same surface glycoproteins have been modeled as receptors for antibody molecules and in the binding of lectin molecules, such as concanavalin A. On the lymphocyte membrane,... 

A FIGURE 17-34 Transcytosis of maternal IgG immunoglobulins across the intestinal epithelial cells of newborn mice. This transcellular movement of a ligand involves both endocytosis and exocytosis. The one-way movement of ligand from the intestinal lumen to the blood depends on the differential affinity of the Fc receptor for antibody at pH 6 (strong binding) and at pH 7 (weak binding). Transcytosis in the opposite direction returns the empty Fc receptor to the luminal membrane. See text for discussion. 

A critical step in radioprotection involves the IL-1 receptors. Monoclonal antibodies to the type 1 IL-1 receptor block IL-l-induced radioprotection (167). Although this receptor is not present on BM cells, it is present on fibroblasts, which suggests that the effects of IL-1 on stem cells maybe largely indirect and mediated by stromal cell activation (168). Anti-IL-1 receptor (type 1) also sensitizes normal mice to the effects of TBI, which suggests that endogenous IL-1 has an intrinsic radioprotective role. IL-6 induction by IL-1, but not CSF levels, is inhibited, which supports the concept that G-CSF and GM-CSF are insufficient by themselves at radioprotecting stem cells and indicates a contributory role for IL-6. Anti-IL-6 antibody blocks IL-1 and TNF-induced radioprotection and also decreases the intrinsic radioresistance of mice, as does anti-TNF- a (169). 

Figure 15.22 T-cell receptor stucture shown as a ribbon diagram. The anbgen-binding site is formed by CDR loops (labeled 1 to 3) from the Va and Vp domain, as for antibodies.

Large granular lymphocytes, not belonging to either the T- or B-cell lineage. Natural killer (NK) cells are considered part of the innate defense system since, in contrast to cytotoxic T-cells, they are able to kill certain tumor cells in vitro without prior sensitization. The basal activity of NIC cells increases dramatically following stimulation with type I IFNs. In addition, NK cells display Fc-receptors for IgG and are important mediators of Antibody-Dependent-Cell-mediated-Cytotoxicity (ADCC). 

Masiero S, Del Vecchio C, Gavioh R, Mattiuzzo G, Cusi MG, Micheli L, Gennari F, Siccardi A, Marasco WA, Palu G, Parolin C (2005) T-cell engineering by a chimeric T-ceU receptor with antibody-type specificity for the HlV-1 gpl20. Gene Ther 12 299-310... 

The principle underlying the BAT is that the attachment of the antigen to the IgE present on the surface of the basophil leads to the activation of the basophil and the release of its mediators (histamine, leukotrienes, prostaglandins, etc.) and the expression on its membrane of molecules such as CD63, CD203c or others which are markers of basophil activation. The basophils are identified with monoclonal antibodies marked with fluorochromes and anti-IgE and anti-CD63 receptors [for a complete review, we suggest readers read references 19-22]. 

Receptors for Fc fragments of IgGs 1 Bind Fc fragments of IgG molecules Target antigen-antibody complexes to myeloid and lymphoid cells, eliciting phagocytosis and other responses... 

Microorganisms are more readily phagocytosed when coated with antibody (opsonized). This is due to the presence on the white blood cells of receptors for the Fc fragment ofIgM and IgG (discussed in Chapter 14). Avoidance of opsonization will clearly enhance the chances of survival of a particular pathogen. A substance called... 

NK cells possess a receptor for Fc/and this enables them to adhere to target cells coated in antibody with the resultant destruction ofthat cell. This phenomenon is known as antibody-dependent cell-mediated cytotoxicity (ADCC). This was attributed to a separate cell population known as killer (K) cells but these have now been shown to be in effect NK cells. 

Types of autoimmune diseases vary widely, from organ-specific diseases such as thyroiditis where there may be stimulation (thyrotoxicosis) by antibody against the receptor for pituitary thyroid-stimulating hormone (TSH) or inhibition (myxoedema) by cell destruction probably mediated by NK cells and autoantibody, through to non-... 

Fc,RI High affinity receptor for IgE Fc,RII Low affinity receptor for IgE FcR Receptor for Fc region of antibody... 

Patients receiving amiodarone must receive monitoring for thyroid abnormalities. Baseline measurements of serum TSH, FT4, FT3, antithyroid peroxidase antibody (anti-TPOAb) and TSH receptor-stimulating antibodies (TSHR-SAb) should be performed. TSH, FT4, and FT3 should be checked 3 months after initiation of amiodarone and then every 3 to 6 months. 

A cardinal role for IL-4 in host protection against intestinal nematode infection was first shown in the H. polygyrus challenge model. Worm expulsion was delayed following treatment with anti-IL-4 or anti-IL-4 receptor monoclonal antibodies, while control treated animals successfully cleared infection (Urban et al., 1991b). Blockade of the IL-4 receptor effectively prevents the in vivo function of IL-4 and IL-13, as these two cytokines share the IL-4 receptor a-chain for signalling functions (Lin et al, 1995). In... 

The involvement of mast cells in host protection against nematode infection is well characterized in T. spiralis infection. W/Wv mice exhibited a significant delay in worm expulsion, and treatment with either anti-SCF or anti-SCF receptor monoclonal antibody dramatically inhibited mast cell responses and expulsion of T. spiralis for the duration of treatment (Donaldson et al., 1996). W/Wv mice also lack interstitial cells of cajal and intraepithelial y T cells (Maeda et al., 1992 Puddington et al., 1994), which may contribute to the impaired response in these animals (see below). However, supporting evidence of a role for mast cells in protection against T. spiralis comes from studies in which overexpression of IL-9 in mice (which is known to influence the mast cell responses see above) resulted in an extremely rapid mast cell-dependent expulsion of T. spiralis (Faulkner et al., 1997). 

Xu et al. [5] described the effect of (z>)-penicillamine on the binding of several antiacetylcholine receptor monoclonal antibodies to the Torpedo acetylcholine receptor. Penicillamine is covalently incorporated into the acetylcholine receptor through SS exchange at the cysteine residues of the a-subunit, altering the antigenic structure of the receptor. This effect on the structure of the native receptor at the neuromuscular junction may be responsible for the establishment of the autoimmune response to the acetylcholine receptor in (i))-penicillamine-induced myasthenia gravis. Cysteine and penicillamine interact to form penicillamine-cysteine mixed disulfide complexes [6] ... 

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