Cellular reaction to group A beta-haemolytic streptococcal membrane antigen and its relation to complement levels in patients with rheumatic heart disease. 1977

R P Sapru, and N K Ganguly, and S Sharma, and R E Chandani, and A K Gupta

Cell-mediated immunity and blood complement activities were studied in 35 patients with chronic rheumatic heart disease (RHD) and 17 normal subjects. The T-cell population in patients with RHD was reduced, as were the CH50 and C3 complement levels. The response to phytohaemagglutinin stimulation was deficient, but the lymphocytes of patients with RHD showed increased avidity for 3H-thymidine when stimulated with specific streptococcal membrane antigen. No differences were found between patients with acute rheumatic activity and those without such activity. The susceptibility of individual patients may be related to the specific sensitisation of lymphocytes, while the fact that this persisted even when T-cell numbers had returned to normal may account for the well-known recrudescenses after streptococcal infections in these patients.

UI MeSH Term Description Entries
D007111 Immunity, Cellular Manifestations of the immune response which are mediated by antigen-sensitized T-lymphocytes via lymphokines or direct cytotoxicity. This takes place in the absence of circulating antibody or where antibody plays a subordinate role. Cell-Mediated Immunity,Cellular Immune Response,Cell Mediated Immunity,Cell-Mediated Immunities,Cellular Immune Responses,Cellular Immunities,Cellular Immunity,Immune Response, Cellular,Immune Responses, Cellular,Immunities, Cell-Mediated,Immunities, Cellular,Immunity, Cell-Mediated,Response, Cellular Immune
D007958 Leukocyte Count The number of WHITE BLOOD CELLS per unit volume in venous BLOOD. A differential leukocyte count measures the relative numbers of the different types of white cells. Blood Cell Count, White,Differential Leukocyte Count,Leukocyte Count, Differential,Leukocyte Number,White Blood Cell Count,Count, Differential Leukocyte,Count, Leukocyte,Counts, Differential Leukocyte,Counts, Leukocyte,Differential Leukocyte Counts,Leukocyte Counts,Leukocyte Counts, Differential,Leukocyte Numbers,Number, Leukocyte,Numbers, Leukocyte
D008213 Lymphocyte Activation Morphologic alteration of small B LYMPHOCYTES or T LYMPHOCYTES in culture into large blast-like cells able to synthesize DNA and RNA and to divide mitotically. It is induced by INTERLEUKINS; MITOGENS such as PHYTOHEMAGGLUTININS, and by specific ANTIGENS. It may also occur in vivo as in GRAFT REJECTION. Blast Transformation,Blastogenesis,Lymphoblast Transformation,Lymphocyte Stimulation,Lymphocyte Transformation,Transformation, Blast,Transformation, Lymphoblast,Transformation, Lymphocyte,Activation, Lymphocyte,Stimulation, Lymphocyte
D002908 Chronic Disease Diseases which have one or more of the following characteristics: they are permanent, leave residual disability, are caused by nonreversible pathological alteration, require special training of the patient for rehabilitation, or may be expected to require a long period of supervision, observation, or care (Dictionary of Health Services Management, 2d ed). For epidemiological studies chronic disease often includes HEART DISEASES; STROKE; CANCER; and diabetes (DIABETES MELLITUS, TYPE 2). Chronic Condition,Chronic Illness,Chronically Ill,Chronic Conditions,Chronic Diseases,Chronic Illnesses,Condition, Chronic,Disease, Chronic,Illness, Chronic
D003165 Complement System Proteins Serum glycoproteins participating in the host defense mechanism of COMPLEMENT ACTIVATION that creates the COMPLEMENT MEMBRANE ATTACK COMPLEX. Included are glycoproteins in the various pathways of complement activation (CLASSICAL COMPLEMENT PATHWAY; ALTERNATIVE COMPLEMENT PATHWAY; and LECTIN COMPLEMENT PATHWAY). Complement Proteins,Complement,Complement Protein,Hemolytic Complement,Complement, Hemolytic,Protein, Complement,Proteins, Complement,Proteins, Complement System
D003176 Complement C3 A glycoprotein that is central in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. C3 can be cleaved into COMPLEMENT C3A and COMPLEMENT C3B, spontaneously at low level or by C3 CONVERTASE at high level. The smaller fragment C3a is an ANAPHYLATOXIN and mediator of local inflammatory process. The larger fragment C3b binds with C3 convertase to form C5 convertase. C3 Complement,C3 Precursor,Complement 3,Complement C3 Precursor,Complement Component 3,Precursor-Complement 3,Pro-C3,Pro-Complement 3,C3 Precursor, Complement,C3, Complement,Complement, C3,Component 3, Complement,Precursor Complement 3,Precursor, C3,Precursor, Complement C3,Pro C3,Pro Complement 3
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000942 Antigens, Bacterial Substances elaborated by bacteria that have antigenic activity. Bacterial Antigen,Bacterial Antigens,Antigen, Bacterial
D012214 Rheumatic Heart Disease Cardiac manifestation of systemic rheumatological conditions, such as RHEUMATIC FEVER. Rheumatic heart disease can involve any part the heart, most often the HEART VALVES and the ENDOCARDIUM. Bouillaud Disease,Bouillaud's Disease,Bouillauds Disease,Disease, Bouillaud,Disease, Bouillaud's,Disease, Rheumatic Heart,Diseases, Rheumatic Heart,Heart Disease, Rheumatic,Heart Diseases, Rheumatic,Rheumatic Heart Diseases
D013297 Streptococcus pyogenes A species of gram-positive, coccoid bacteria isolated from skin lesions, blood, inflammatory exudates, and the upper respiratory tract of humans. It is a group A hemolytic Streptococcus that can cause SCARLET FEVER and RHEUMATIC FEVER. Flesh-Eating Bacteria,Streptococcus Group A,Bacteria, Flesh-Eating

Related Publications

R P Sapru, and N K Ganguly, and S Sharma, and R E Chandani, and A K Gupta
February 1983, The Indian journal of medical research,
R P Sapru, and N K Ganguly, and S Sharma, and R E Chandani, and A K Gupta
February 1983, The Indian journal of medical research,
R P Sapru, and N K Ganguly, and S Sharma, and R E Chandani, and A K Gupta
December 1987, Japanese circulation journal,
R P Sapru, and N K Ganguly, and S Sharma, and R E Chandani, and A K Gupta
April 2024, BMJ (Clinical research ed.),
R P Sapru, and N K Ganguly, and S Sharma, and R E Chandani, and A K Gupta
January 1965, Nature,
R P Sapru, and N K Ganguly, and S Sharma, and R E Chandani, and A K Gupta
September 1981, The Journal of clinical investigation,
R P Sapru, and N K Ganguly, and S Sharma, and R E Chandani, and A K Gupta
February 1971, The Medical journal of Australia,
R P Sapru, and N K Ganguly, and S Sharma, and R E Chandani, and A K Gupta
May 1969, Bulletin on the rheumatic diseases,
R P Sapru, and N K Ganguly, and S Sharma, and R E Chandani, and A K Gupta
July 1985, Thorax,
R P Sapru, and N K Ganguly, and S Sharma, and R E Chandani, and A K Gupta
January 1962, Reumatismo,
Copied contents to your clipboard!