Erythrocyte with antigen

Many microorganisms minimize the effects of the host s defence system against them by mimicking the antigenic stmcture of the host tissne. The eventual immunological response of the host to infection then leads to the autoimmune destmction of itself. Thus, infections with Mycoplasma pneumoniae can lead to production of antibody against normal Group 0 erythrocytes with concomitant haemolytic anaemia. 

Autoantibodies to red blood cells and autoimmune hemolytic anemia have been observed in patients treated with numerous drugs, including procainamide, chlor-propaminde, captopril, cefalexin, penicillin, and methyldopa (Logue et al., 1970 Kleinman et al., 1984). Hydralazine- and procainamide-induced autoantibodies may also result in SLE. Approximately 20% of patients administered methyldopa for several weeks for the treatment of essential hypertension developed a dose-related titer and incidence of autoantibodies to erythrocytes, 1% of which presented with hemolytic anemia. Methlydopa does not appear to act as a hapten but appears to act by modifying erythrocyte surface antigens. IgG autoantibodies then develop against the modified erythrocytes. 

If a fixed amount of antigen is labeled by combining it with erythrocytes i.e., if the red blood cells are coated with antigen (B7), the... 

Reed, M. B., Caruana, S. R., Batchelor, A. H., Thompson, J. K., Crabb, B. S., and Cowman, A. F. (2000). Targeted disruption of an erythrocyte binding antigen in Plasmodium falciparum is associated with a switch toward a sialic add-independent pathway of invasion. Proc. Natl. Acad. Sci. USA 97, 7509-7514. 

Gallium arsenide has been shown to be an immunosuppressant. When administered intratracheally to mice at concentrations between 50 and 200 mg kg GaAs suppressed the in-vivo antibody-forming cell (AFC) response to sheep erythrocytes (SRBC), and interfered with antigen processing that is essential for CD4+ T-cell stimulation by splenic macrophages (Sikor-ski etal. 1991, Lewis TA etal. 1996). The arsenic moiety appears to be responsible... 

Treatment of erythrocytes with neuraminidase increased their antibody affinities for the antigenic receptors. In contrast, the use of proteolytic enzymes, in removing glycopeptide chains, greatly diminishes steric hindrance and brings about higher affinity constants. 

Athanassiades (1981) published a more comprehensive study also using sheep erythrocytes as antigen. Four different retinoids were tested, all in subtoxic doses retinyl palmitate, motretinid (F3), etretinate, and 13-cw-retinoic acid. All retinoids, with the exception of etretinate, stimulated DTH when injected together with the sensitizing antigen. This protocol had not been used in our experiments, which may explain our negative results. To date, this is the only... 

The complement system has the ability to combine irreversibly with antigen-antibody complexes. If the antigen is a protein component of the sheep erythrocyte cell surface, this combination induces lysis of the erythrocyte and thus offers an excellent quantitative indication of complement fixation. After incubation of the complement with the antigen-antibody complex under study, its fixation is studied by evaluating its residual haemolytic activity when the lytic antigen-antibody system is added. Since the concentrations of antibodies in the first system and of complement remain constant, haemolysis will be inversely proportional to the amoimt of antigen added to the incubation mixture (Table 1). 

Figure 11.30 Adjuvant effect of nano-encapsulated human immunogammaglobulin-G (IgG). Antigens with various adjuvants and untreated. Immunization of guinea-pigs after subcutaneous application of IgG. Antibody formation against IgG measured with a passive agglutination test (haemagglutination microtechnique) from guinea-pig serum with antigen-sensibilized sheep erythrocytes. The adjuvant effect of nano-encapsulated IgG compared to a classical Al203lgG adsorbate is evident. From Speiser [186].

Drugs frequently bind to blood elements directly (e.g. penicillin to erythrocytes) and the antibodies to the resultant complex react with, and damage, cells coated with the drug. Viruses, especially those that bud, become associated with the host cell surface antigens with the resultant generation of Tc cells. 

Erythrocytes are labeled with cell surface antigens that determine blood type. Two types of inherited antigens are found on red blood cells A antigens and B antigens. Accordingly, four blood types are possible (see Table 16.1) ... 

If blood from blood group A is transfused into the circulation of an individual with blood group B, for example, then the anti-A present there binds to the A antigens. The donor erythrocytes marked in this way are recognized and destroyed by the complement system (see p. 298). In the test tube, agglutination of the erythrocytes can be observed when donor and recipient blood are incompatible. 

The rhesus D antigen occurs in 84% of all white individuals, who are therefore Rh-pos-itive. If an Rh-positive child is born to an Rh-negative mother, fetal erythrocytes can enter the mother s circulation during birth and lead to the formation of antibodies (IgG) against the D antigen. This initially has no acute effects on the mother or child. Complications only arise when there is a second pregnancy with an Rh-positive child, as maternal anti-D antibodies cross the placenta to the fetus even before birth and can trigger destruction of the child s Rh-positive erythrocytes [fetal erythroblastosis). 

The IgD profile in a normal Nigerian population was similar to that of the British and American populations (T7). Interestingly, in more than half the patients with African trypanosomes, IgD was absent from their sera (M35). Three out of six diabetic patients had insulin antibodies of the IgD class (D3), and IgD levels were five to six times higher in Ethiopian children than in Swedish children of the same age (J4). Patients with penicillin-induced hemolytic anemia had IgD receptors on their erythrocyte surfaces and sera from some subjects allergic to penicillin G were shown to have IgD antibodies specific for the benzyl-penicilloyl-antigenic determinant of this antibiotic (C19). 

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