mimmunМедицинская иммунологияMedical Immunology (Russia)1563-06252313-741XSPb RAACI10.15789/1563-0625-CRI-2029mimmun-2029Research ArticleОБЗОРЫREVIEWSРецептор CD32а и его роль в норме и при патологииCD32a receptor in health and diseaseАрсентьеваН. А.ArsentievaN. A.

Арсентьева Наталья Александровна – к.б.н., старший научный сотрудник

197101, Санкт-Петербург, ул. Мира, 14.Teл.: 8 (904) 646-57-58.

Arsentieva Natalia A. – PhD (Biology), Senior Research Associate

197101, St. Petersburg, Mira str., 14.Phone: 7 (904) 646-57-58.

arsentieva_n.a@bk.ruБацуновО. К.BatsunovO. K.

младший научный сотрудник ФБУН «Санкт-Петербургский научно-исследовательский институт эпидемиологии и микробиологии имени Пастера»; старший лаборант кафедры иммунологии ФГБОУ ВО «Первый Санкт-Петербургский государственный медицинский университет имени академика И.П. Павлова» Министерства здравоохранения РФ

Санкт-Петербург

Junior Research Associate, Pasteur Research Institute of Epidemiology and Microbiology; Senior Laboratory Assistant, Department of Immunology, Pavlov University

St. Petersburg

batsunov@gmail.comКудрявцевИ. В.KudryavtsevI. V.

к.б.н., доцент кафедры иммунологии ФГБОУ ВО «Первый Санкт-Петербургский государственный медицинский университет имени академика И.П. Павлова» Министерства здравоохранения РФ; заведующий отделом иммунологии ФГБНУ «Институт экспериментальной медицины»

Санкт-Петербург

PhD (Biology), Assistant Professor, Department of Immunology, First St. Petersburg State I. Pavlov Medical University; Head, Department of Immunology, Institute of Experimental Medicine

St. Petersburg

igorek1981@yandex.ruСемёновА. В.SemenovA. V.

д.б.н., заместитель директора по инновационной работе ФБУН «Санкт-Петербургский научно-исследовательский институт эпидемиологии и микробиологии имени Пастера»; профессор кафедры иммунологии ФГБОУ ВО «Первый Санкт-Петербургский государственный медицинский университет имени академика И.П. Павлова» Министерства здравоохранения РФ

Санкт-Петербург

PhD, MD (Biology), Deputy Director for Innovation, Pasteur Research Institute of Epidemiology and Microbiology; Professor, Department of Immunology, First St. Petersburg State I. Pavlov Medical University

St. Petersburg

alexvsemenov@yahoo.comТотолянАрег А.TotolianAreg A.

д.м.н., профессор, академик РАН, директор ФБУН «Санкт-Петербургский научно-исследовательский институт эпидемиологии и микробиологии имени Пастера»; заведующий кафедрой иммунологии ФГБОУ ВО «Первый Санкт-Петербургский государственный медицинский университет имени академика И.П. Павлова» Министерства здравоохранения РФ

Санкт-Петербург

PhD, MD (Medicine), Professor, Full Member, Russian Academy of Sciences, Director, Pasteur Research Institute of Epidemiology and Microbiology; Head, Department of Immunology, First St. Petersburg State I. Pavlov Medical University

St. Petersburg

totolian@spbraaci.ruФБУН «Санкт-Петербургский научно-исследовательский институт эпидемиологии и микробиологии имени Пастера»РоссияPasteur Research Institute of Epidemiology and MicrobiologyRussian FederationФБУН «Санкт-Петербургский научно-исследовательский институт эпидемиологии и микробиологии имени Пастера»; ФГБОУ ВО «Первый Санкт-Петербургский государственный медицинский университет имени академика И.П. Павлова» Министерства здравоохранения РФРоссияPasteur Research Institute of Epidemiology and Microbiology; First St. Petersburg State I. Pavlov Medical UniversityRussian FederationФГБОУ ВО «Первый Санкт-Петербургский государственный медицинский университет имени академика И.П. Павлова» Министерства здравоохранения РФ; ФГБНУ «Институт экспериментальной медицины»РоссияFirst St. Petersburg State I. Pavlov Medical University; Institute of Experimental MedicineRussian Federation202020052020223433442Copyright © Арсентьева Н.А., Бацунов О.К., Кудрявцев И.В., Семёнов А.В., Тотолян А.А., 20202020Арсентьева Н.А., Бацунов О.К., Кудрявцев И.В., Семёнов А.В., Тотолян А.А.Arsentieva N.A., Batsunov O.K., Kudryavtsev I.V., Semenov A.V., Totolian A.A.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.mimmun.ru/mimmun/article/view/2029

Низкоаффинные Fcγ-рецепторы, ответственные за распознавание Fc-фрагмента молекул иммуноглобулинов (Ig), обычно в связанном с антигеном состоянии, являются связующим звеном между врожденным и гуморальным иммунитетом. Они играют значимую роль при воспалительных и инфекционных заболеваниях. Среди них выделяют отдельное семейство FcγRII (СD32), особенностью которого является передача внутриклеточного сигнала независимо от общей γ-цепи, они имеют одну α-цепь, содержащую 2 внеклеточных иммуноглобулиноподобных домена. Рецепторы FcγRII представлены практически на всех клетках врожденного иммунитета: моноцитах и макрофагах, нейтрофилах, эозинофилах, дендритных клетках, а также В-лимфоцитах и тромбоцитах. Они выполняют две основные функции: обеспечивают распознавание, облегчают фагоцитоз и разрушение моноцитами/макрофагами опсонизированных антителами клеток (в том числе патогенных); параллельно происходит активация фагоцитов, путем стимуляции синтеза цитокинов. Среди членов FcγRII семейства присутствуют активационные FcγRIIA (CD32a) и FcγRIIC (CD32c) и ингибирующие FcγRIIB (CD32b) рецепторы. Рецепторы FcγRII с низкой аффинностью связываются с IgG, естественными лигандами для них являются иммунные комплексы. Высокие уровни иммунных комплексов обычно обнаруживаются как при хронических вирусных инфекциях, так и при аутоиммунных заболеваниях. Известны полиморфные варианты гена CD32а, которые могут приводить к изменению функции рецептора и, тем самым обуславливать различную восприимчивость к инфекциям, влиять на развитие аутоиммунных заболеваний и первичных иммунодефицитных состояний. Активация рецептора CD32a индуцирует выработку провоспалительных цитокинов, включая TNFα и интерферонов, которые участвуют в воспалении при системной красной волчанке, болезни Кавасаки, болезни Грейвса и ревматоидном артрите. Показано, что посредством рецептора CD32a осуществляется антибактериальная активность тромбоцитов. Особый интерес вызвало исследование экспрессии CD32a у людей, инфицированных вирусом иммунодефицита человека (ВИЧ). Рецептор CD32a претендует на роль биомаркера клеток, являющихся резервуаром ВИЧ-инфекции. Однако на сегодняшний день остается много вопросов относительно механизмов экспрессии CD32a на ВИЧ-инфицированных клетках и роли CD32a в формировании резервуара ВИЧ и/или развития резистентности. Помимо ВИЧинфекции, показано значение рецепторов FcγR в других инфекционных заболеваниях, например при инфекции, вызванной вирусом гриппа и лихорадки денге. Лучшее понимание структуры и функции этого рецептора поможет оценить его роль в иммунопатогенезе заболеваний. Настоящий обзор сосредоточен на роли CD32a в развитии иммунного ответа в норме и при различных заболеваниях.

Low-affinity Fcγ-receptors that recognize the Fc portion of immunoglobulin (Ig) molecules, usually being in antigen-bound state, thus representing a link between innate and adaptive immunity. They play a significant role in inflammatory and infectious diseases. Among them, a separate FcγRII family (CD32) is discerned, which is characterized by transmission of intracellular signal independently of the common γ-chain, they have one α-chain containing two extracellular immunoglobulin-like domains. FcγRII receptors are present in almost all cells of the innate immune system: monocytes and macrophages, neutrophils, eosinophils, dendritic cells, as well as on B-lymphocytes and platelets. They perform two main functions: target recognition, facilitation of phagocytosis and destruction of antibody-opsonized cells by monocytes/ macrophages (including pathogenic cells). In parallel, the phagocytes are activated via the cytokine synthesis stimulation. The FcγRIIA (CD32a) and FcγRIIC (CD32c) activating receptors, like as FcγRIIB (CD32b) inhibiting receptors are present among the members of the FcγRII family. The low-affinity FcγRII receptors bind to IgG, with immune complexes being their natural ligands. High levels of immune complexes are usually found in both chronic viral infections and autoimmune diseases. There are shown polymorphic variants of the CD32a gene, which can affect the receptor function, and, thereby, causing susceptibility for different infections, influence the development of autoimmune diseases and primary immunodeficiencies. Activation of the CD32a receptor induces the production of pro-inflammatory cytokines, including TNFα and interferons, that are involved into inflammation in systemic lupus erythematosus, Kawasaki disease, Graves’ disease and rheumatoid arthritis. It has been shown that antibacterial activity of platelets is carried out via the CD32a receptor. The study of CD32a expression in people The CD32a receptor is considered a biomarker of cells that are a reservoir of HIV infection. At the present time, however, many questions remain regarding the mechanisms of CD32a expression of on HIV-infected cells and the role of CD32a in the formation of an HIV reservoir and/or development of appropriate resistance. In addition to HIV infection, the significance of FcγR receptors is shown in other infectious diseases, for example, with influenza and dengue virus infections. Better understanding of the CD32a structure and function will help to assess its role in immunopathogenesis of different conditions. This review focuses on the role of CD32a in development of the normal immune response in normal state and various diseases.

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The authors declare that there are no conflicts of interest present.