Upregulation of CD32 in T cells from infants with severe RSV disease: a new costimulatory pathway?

SANANEZ I; RAIDEN S; HOLGADO P; SEERY V; DE LILLO L; DAVENPORT C; FERRERO FERNANDO; PEEPLES M; GEFFNER J; ARRUVITO L

AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY

AMER THORACIC SOC

Lugar: New York; Año: 2020

1044-1549

Respiratory syncytial virus (RSV) infection is a major cause of severe respiratory disease in infants, immunocompromised and older adults. RSV infects virtually all children by 2-3 years of age, resulting in nearly 3 million hospitalizations and 100,000 in-hospital deaths annually, mostly in developing countries (1). There is no approved vaccine against RSV infection. Passive prophylaxis with the anti-RSV antibody, palivizumab, is the only intervention licensed for the prevention of severe RSV disease in high-risk individuals (2, 3). RSV-specific serum IgG antibodies are present in most children and adults, reflecting the universality of RSV infection throughout life. Neutralizing antibodies remain a commonly accepted measure of protective immunity in vaccine trials (4). However, IgG antibodies might influence the course of RSV disease not only by acting as neutralizing antibodies, but also by activating effector functions through the receptors for the Fc portion of IgG (FcRs) (5, 6). These receptors are widely expressed in myeloid and B cells. Whether T cell express FcRs is still controversial, but recent studies strongly suggest that a minor fraction of T cells expresses FcRII (CD32) (7-10). We here show that severe RSV infection in infants is associated with a marked upregulation of CD32 on T cells. Moreover, we found that CD32 ligation improves the activation of CD4+ and CD8+T cells from hospitalized infants.