हमारा समूह 1000 से अधिक वैज्ञानिक सोसायटी के सहयोग से हर साल संयुक्त राज्य अमेरिका, यूरोप और एशिया में 3000+ वैश्विक सम्मेलन श्रृंखला कार्यक्रम आयोजित करता है और 700+ ओपन एक्सेस जर्नल प्रकाशित करता है जिसमें 50000 से अधिक प्रतिष्ठित व्यक्तित्व, प्रतिष्ठित वैज्ञानिक संपादकीय बोर्ड के सदस्यों के रूप में शामिल होते हैं।
ओपन एक्सेस जर्नल्स को अधिक पाठक और उद्धरण मिल रहे हैं
700 जर्नल और 15,000,000 पाठक प्रत्येक जर्नल को 25,000+ पाठक मिल रहे हैं
Sarkar S ,Rastogi M ,Kumar R ,Chakraborti A *
The autoimmune sequelae of rheumatic fever (RF) and rheumatic heart disease (RHD) are due to untreated or partially treated pharyngitis caused by Group A streptococcus (GAS). RF/RHD usually affects the genetically susceptible individuals. KIR (Killer cell immunoglobulin like receptor) of NK (natural killer) cell has been documented in susceptibility to various autoimmune diseases. KIR is of activating, inhibitory, pseudo and framework types. In here, 29 patients (pharyngitis, RF and RHD) and controls were studied to establish the association of different KIR genes in development of RF/RHD. KIR genotyping in all the disease groups revealed that the frequency of activating KIR2DS4A and inhibitory KIR2DL5B were less in RHD compared to the control. On the other hand, frequency of activating KIR2DS5A was more in RHD than pharyngitis. A significant difference in the frequency of KIR2DS2A and KIR3DL1B were found in pharyngitis compared to control. Interestingly, the overall data revealed a marked decrease of activating genes in pharyngitis and an increase in RHD. However, in the study, the framework genes were comparatively conserved and pseudo genes did not show any significant change. Thus, the study suggests an association of KIR in the pathogenesis of RF/RHD by demonstrating the variations in specific genotypes. This can be correlated to the prolonged activation of NK cells which may be accountable for regulation of adaptive immune response and self-tolerance. Further study in large cohort may unveil more information regarding the role of KIR in the development of the disease.