Diseases association with the polymorphic major histocompatibility complex class I related chain a: MICA gene

The Major Histocompatibility Complex class I chain-related molecule A (MICA) genes encode a highly polymorphic glycoprotein among the cell surface antigens that trigger an immune response after allograft transplantation. It is encoded by the MICA gene, a member of the glycosylated MIC genes. Discovered in 1994, the MICA gene is located within the MHC class I region. Moreover, its biological function is achieved through the interaction with the NKG2D receptor. Unlike the classical HLA molecules, MICA protein is not associated with β2- microglobulin nor binds peptides. MICA gene expression may result in a cytotoxic response and IFN-γ secretion through the up-regulation by heat shock proteins in response to infection (Human Cytomegalovirus HCMV), mediated by NKG2D-expressing cells. Anti-MICA antibodies were identified as significant risk factors for antibody mediated rejection after being detected in sera of patients with graft rejection. In addition, soluble MICA proteins (sMICA) has been detected in the serum of transplant recipients with cancers. Furthermore, the association of MICA polymorphisms with infectious diseases, various autoimmune diseases, cancer, and allograft rejection or graft-versus-host disease (GVHD) has been studied. Moreover, numerous advanced disease studies centered on MICA polymorphism are independent of HLA association. In this review, we discussed the up-to-date data about MICA and the association of MICA polymorphism with infections, autoimmune diseases, graft-versus-host disease, and cancer.     

The major histocompatibility complex of the rat

Immunogenetic studies in the rat began with the investigation of blood group antigens (1-7) and evolved into the investigation of histocompatibility antigens and transplantation phenomena (8-17). In the course of this work, several nomenclature systems evolved that were eventually reconciled in a series of comparison studies (18-24). The biennial Workshops on Alloantigenic Systems in the Rat held under the aegis of the Transplantation Society (24) have provided the forum for the continued evolution of this field. In addition, several reviews (24-31) and books (32-35) have provided periodic summaries of different aspects of rat immunogenetics. This review will focus on the structure of the major histocompatibility complex (MHC) of the rat from the serological, biochemical, and molecular points of view.     

Congenital abnormalities of the lower urinary tract: infravesical anomalies

Abnormalities of the lower urinary tract may range from frequent and very minor with no significant consequences to the rare but severe requiring major intervention and lifelong monitoring. While discussion of all infravesical congenital abnormalities of the lower urinary tract is beyond the scope of this article, the main abnormalities encountered in clinical practice are listed and discussed.     

Transplantation in miniature swine. I. Fixation of the major histocompatibility complex.

Three strains of miniature swine, each homozygous for a different allele of the major histocompatibility locus (MHC), have been developed by a selective breeding scheme based on tissue typing of the offspring of each generation. Prior to breeding, the original parents were reciprocally immunized by skin grafts and lymphocyte injections to produce lymphocytotoxic antisera. These antisera were then used to assess the MHC genotype of the offspring by an analysis based on selective absorption of cytotoxicity. Offspring inheriting the same serologically determined genotype were then bred sequentially. Subsequent mixed lymphocyte cultures showed a pattern of reactivity consistent with the serological genotyping, further confirming the homology between the MHC of these miniature swine and those of man and mouse. In addition to their usefulness as a model for large animal surgical transplantation, these animals provide an abundant homozygous source of histocompatibility antigens and of antihistocompatibility antisera for use in chemical characterization of products of the MHC.     

Lower urinary tract reconstruction in association with renal transplantation

Congenital or acquired dysfunction of the lower urinary tract may result in renal failure. In this group of patients urinary diversion or lower urinary tract reconstruction is mandatory prior to renal transplantation. Avoiding creation of an external stoma offers far more better quality of life to these unfortunate patients. We present three patients in end-stage renal disease. Two of them presented with dysfunction of the lower urinary tract and the third with absence of the bladder. Reconstruction or substitution of their bladders has been performed prior to kidney transplantation. In one patient an artificial urinary sphincter was implanted simultaneously in order to achieve continence, while all the patients have to empty their neobladders or augmented bladders by clean intermittent self-catheterization. In conclusion, dysfunction or absence of the lower urinary tract does not preclude renal transplantation and however abnormal the urinary tract, transplantation can still be performed if low-pressure, high-compliance reservoir can be achieved by means of augmentation or substitution cystoplasty.     

Symptomatic urinary problems in female genital tract anomalies

Most of urological abnormalities in urogenital anomalies are asymptomatic and need no special treatment; however, a few patients have critical urinary complaints and surgical corrections are required for them. Unfortunately, these coexisting urinary problems are often neglected and failed to be treated. So, it is necessary to delineate the diagnosis and treatment of similar anomalies. Eight typical patients who had urogenital anomalies with urinary discomfort in our institution were excerpted and reported. In this series, the urinary symptoms ranged from cyclical hematuria and urinary incontinence to infection symptom. The involved urological anatomies were generally categorized into three types: abnormal communication of urogenital tracts, malformation of bladder or ectopic ureter, and anomalies of urethral orifice. Surgical corrections were helpful for most cases. For patients with genitalia anomalies, the coexisting urological defects should be highlighted by our gynecologists, especially when they are symptomatic and require surgical correction. Shu Wang and Jing He Lang contributed equally to this article.