Keerthivasan, S., Şenbabaoğlu, Y., Martinez-Martin, N., Husain, B., Verschueren, E., Wong, A., Yang, Y. A., Sun, Y., Pham, V., Hinkle, T., Oei, Y., Madireddi, S., Corpuz, R., Tam, L., Carlisle, S., Roose-Girma, M., Modrusan, Z., Ye, Z., Koerber, J. T., & Turley, S. J. (2021). Homeostatic functions of monocytes and interstitial lung macrophages are regulated via collagen domain-binding receptor LAIR1. Immunity, 54(7), 1511-1526.e8. https://doi.org/10.1016/j.immuni.2021.06.012

Suggested mechanism for this is via Spike protein binding TLR4, this can be blocked with NFkB and TLR4 inhibitors potentially offering a therapeutic strategy https://doi.org/10.1101/2020.12.18.423427

Additionally SARS-CoV-2 nucleocaspid can drive IL-6 in macrophages https://doi.org/10.3390/vaccines9010054

SLAMF7 'super activation' has been detected in lung infiltrating and monocyte derived macrophages of COVID19 patients resulting in significant upregulation of proinflammatory cytokines https://doi.org/10.1101/2020.11.05.368647 (preprint)

It is not thought that circulating immune cells (i.e. monocytes) become infected with SARS-CoV-2 to a large extent https://doi.org/10.1101/2021.01.19.427282

Additionally, a study showed that SARS-CoV-2 does not readily infect human monocyte derived macrophages nor drive significant cytokine production https://doi.org/10.1101/2020.12.22.423940

However, this is not seen in other studies and the cells primarily thought to be infected would rather be lung alveolar macrophages. These have different receptors, origins (i.e. embryonic vs monocyte perhaps), and are in an in situ setting unlike studies with in vitro-derived monocytic macrophages (6-day culture with only one growth factor). Therefore, this is still unclear.