In a study published in the journal Mucosal Immunology, researchers compared the effects of phagocytosis of HIV-1-infected cells when triggered by virus-specific antibodies, either in the IgA or IgG form. They discovered that phagocytosis mediated by IgA abundant in the mucous membranes, not only destroyed infected cells but also allowed to present viral antigens to CD8+ T lymphocytes and activated their cytotoxic function (their ability to kill infected cells). In contrast, IgG antibodies, more prevalent in the blood, did not produce this effect.
Furthermore, after binding to IgA and triggering phagocytosis of infected cells, monocytes reprogram themselves into activated macrophages. These macrophages exhibit a mixture of pro-inflammatory and anti-inflammatory properties and secrete pro-inflammatory chemokines (molecules that attract other immune cells).
IgA-mediated ADCP also makes monocytes more reactive to a new bacterial infection: they produce more cytokines such as IL-6 and TNFα. This phenomenon is a sign of trained immunity, a recent form of memory in the innate immune system, which allows it to better respond to future attacks.
All these observations show that there is a close link between adaptive (specific) immunity initiated by IgA and innate (natural) immunity.

This discovery opens the way to new strategies to prevent the spread of HIV, by exploiting the protective role of IgA antibodies and their ability to activate both the natural and specific defenses of our body.