Complement receptor 1 (CR1, CD35) serves as a pivotal mediator of erythrocyte immune function, orchestrating processes that range from immune complex clearance to modulation of host-pathogen interactions. CR1's structural heterogeneity, including the F and S allelic forms, contributes to variable receptor expression and clustering, thereby influencing erythrocyte deformability, immune adherence, and susceptibility to pathogen-mediated rosetting (Vik & Wong, 1993; Rowe et al., 1997). The molecular mechanisms underlying CR1 clustering involve complex interactions with cytoskeletal scaffolding proteins such as FAP-1 and ATP-mediated signaling pathways, which enhance receptor aggregation and facilitate efficient immune complex transport (Ghiran et al., 2008; Melhorn et al., 2013). CR1's role extends beyond erythrocyte-mediated clearance, influencing complement-mediated tissue injury in ischemia-reperfusion scenarios, where soluble CR1 demonstrates protective effects against microvascular and myocardial damage (Lindsay et al., 1992; Shandelya et al., 1993).

This review integrates molecular, cellular, and translational perspectives on CR1 function, emphasizing receptor clustering dynamics, immune adherence, and erythrocyte deformability. Theoretical frameworks and historical studies contextualize CR1’s evolution as a critical immune modulator, while contemporary research elucidates the interplay between receptor polymorphisms, ligand binding, and immune signaling pathways. Mechanistic insights from human and animal models reveal the receptor’s dual role in pathogen defense and modulation of complement-mediated injury (Pringle et al., 2012; Sun et al., 2012). Additionally, CR1-targeted interventions, including soluble recombinant constructs, offer therapeutic potential in ischemia-reperfusion injury and infectious disease contexts, underscoring the clinical relevance of receptor modulation (Smith et al., 1993; Chavez-Cartaya et al., 1995).

This article provides a comprehensive synthesis of the CR1 literature, critically evaluating empirical findings, methodological approaches, and theoretical constructs. Emphasis is placed on the implications of receptor clustering for immunological homeostasis, the influence of genetic polymorphisms on receptor functionality, and the translational significance of manipulating CR1 in disease contexts. By integrating cellular, molecular, and clinical perspectives, this review delineates current knowledge gaps and proposes directions for future research, including high-resolution mapping of receptor-ligand interactions, longitudinal assessment of erythrocyte-mediated immune clearance, and therapeutic modulation of complement activity.

It is well known that in recent years infectious diseases have not only caused significant damage to the global economy, but in some cases are also considered capable of threatening other sectors (trade, tourism, social sphere). Among such diseases, African horse sickness (AHS) occupies a special place due to its aggressiveness (mortality rate 90–95%). This disease is transmissible and is spread to equids (horses, donkeys, mules, zebras) through blood-sucking insects. In addition, Culicoides species—C. imicola and C. bolitinos—have been identified as the main vectors (biting midges), which requires a comprehensive approach involving epizootologists, virologists, and entomologists. African horse sickness has not been reported in our country, nor in CIS member states, but due to its high risk, the disease deserves special attention.

This article presents data on the global distribution and existing risks of AHS, as well as the results of the first seromonitoring conducted in the country to prevent the disease in equine species.

As a result of the conducted studies, all samples obtained from a total of 2,687 horses and donkeys showed negative results in the ELISA test.