„Glycosidic exclusion“ does not include the „Oh“ or Bombay Type

The classical <i>Bombay type</i> is characterized by the lack of expression of any ABO(H) epitope and instead shows the development of high isoagglutinin levels, additionally exerting strong binding of complement to anti-H agglutinin. The red cell surface presents with the naked structure Gal-β1-R, which has not been completed for the H-receptor (Fuc-α1-2-Gal-β1-R), thereby representing the structural fundament for ABOH epitopes. In its native form, the <i>Bombay</i> type occurs in individuals with the extremely rare genotype (h/h;se/se). This molecular biological phenomenon is explained by point mutations at the H- and Se genes on chromosome 19 such that the fucosyltransferases FUT1 and FUT2 are not encoded. FUT1 and FUT2 are epistatically connected with the A and B allelic glycotransferase functions encoded on chromosome 9, and fucosyl residues provide the functional-structural basis of the formation of any ABOH phenotype on the cell surface or in secretions and plasma proteins. Moreover, through developmental varying of the positions of the fucosyl residues between the cell surfaces and the heavy chains of immunoglobulins, they appear to augment or reduce antibody-mediated cellular cytotoxicity. This involves the regulation of growth processes and control over physiological autoreactivity in embryonic stem cell to germ cell transformation, where the predominantly <i>O</i>-glycosylations become in <i>Bombay type</i> individuals consequently exposed to metabolic competition with multiple glycosidic sites of extremely glycan depleted immunoglobulins.

经典的孟买血型（Bombay type）以不表达任何ABO(H)表位为特征，反而会产生高水平的同种凝集素，此外还可介导补体与抗H凝集素发生强力结合。其红细胞表面呈现裸露的Gal-β1-R结构，该结构尚未转化为H受体（Fuc-α1-2-Gal-β1-R），而这正是ABOH表位形成的结构基础。天然状态下，孟买血型仅见于携带极为罕见的h/h；se/se基因型的个体。这种分子生物学现象的成因是19号染色体上H基因与Se基因发生点突变，导致无法编码岩藻糖基转移酶FUT1与FUT2。FUT1和FUT2与9号染色体上编码的A、B等位基因糖基转移酶功能存在上位性关联；岩藻糖残基则为细胞表面、分泌物及血浆蛋白上任意ABOH表型的形成提供了功能结构基础。此外，岩藻糖残基在细胞表面与免疫球蛋白重链之间的位置存在发育动态变化，这类变化似乎可增强或减弱抗体介导的细胞毒性。这一过程涉及胚胎干细胞向生殖细胞转化过程中的生长调控与生理性自身反应性控制，而孟买血型个体体内主要的O-糖基化会因此暴露于与糖基极度缺失的免疫球蛋白的多个糖苷位点之间的代谢竞争。