Indica
Backed by cutting edge technology, an uncompromising focus on ease-of-use and dedicated customer service, Indica Labs’ software and services are being used to make vital discoveries in pathology labs and research organizations around the world.
+1 (505) 492 0979
sales: info@indicalab.com
support: support@indicalab.com

Identification of immune checkpoints in COVID-19

Indica Labs / Spotlight on Covid-19 Research Publications  / Identification of immune checkpoints in COVID-19

Identification of immune checkpoints in COVID-19

Carvelli, J., Demaria, O., Vély, F., et al. Identification of immune checkpoints in COVID-19. Please note that this article has not completed peer review. doi: 10.21203/rs.3.rs-27340/v1

Coronavirus disease 2019 (COVID-19) is a new pandemic acute respiratory disease caused by
infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)11-3. We provide here a
longitudinal analysis of immune responses, including immune cell phenotyping and assessments of
the soluble factors present in the blood and broncho-alveolar lavage fluid (BALF) of patients at various
stages of COVID-19 severity: paucisymptomatic, pneumonia and acute respiratory distress syndrome
(ARDS). While we confirm a lymphopenia associated with COVID-19 severity4-7, we report an increase
in expression of the NKG2A and PD-1 inhibitory receptors on T and natural killer (NK) cells, as well as
an increase in CD39 expression on NK cells, suggesting that therapeutic blocking antibodies targeting
these molecules already used for cancer immunotherapy8 could be repurposed as first line of defense
to promote SARS-CoV-2 clearance. In addition, the C5a anaphylatoxin and its receptor C5aR1 (CD88)
play a key role in the initiation and maintenance of inflammatory responses, by recruiting neutrophils
and monocytes to the lungs9,10. We report an increase in soluble C5a levels proportional to COVID-19
severity and high levels of C5aR1 expression in blood and BALF myeloid cells, indicating a potential
role of the C5a-C5aR1 axis in the pathophysiology of ARDS. Avdoralimab is a clinical-stage anti-C5aR1
therapeutic monoclonal antibody (mAb) that prevents C5a-mediated myeloid cell recruitment and
activation. We propose the use of this antibody to limit myeloid cell infiltration in the lung and to
prevent the excessive lung inflammation associated with ARDS in COVID-19 patients.

Click here to access pre-print research paper