Table 1 Cells involved in immunoinflammation of ARDS
| Â | Cell type | Pathological process | Pathological changes | Outcome | Ref |
|---|---|---|---|---|---|
Innate immune-driven immunoinflammation | Macrophage | Polarized into pro-inflammatory phenotypes | Elevated levels of SP-D and anti-spike antibodies | Macrophage dysfunction | |
Phagocytosis is impaired | Increased level of SIRP-alpha | ||||
Efferocytosis is impaired | Elevated levels of HMGB1; VEGF-C/VEGFR-3 signaling pathway | ||||
Monocyte | Aberrant activation | Strong monocyte/DC activation was observed with increasing levels of typical inflammatory markers | Additional innate immune disorder and severe inflammation | ||
DC | |||||
Neutrophils | Produce high level of NETs | Enhanced vascular damage | Severe cytokine storm | ||
Eosinophils | Elevated eosinophil level | Quick response to pulmonary injury | Inflammation | ||
Adaptive immune-driven immunoinflammation | T cells | Overproduction of T lymphocytes | Abundant T cells are detected in the BALF | Hyperimmunoinflammation | |
Activation of unconventional T cells | Highly activated in the airways of patients with CARDS | ||||
Imbalance between effector T lymphocytes and the capacity to present antigens in APCs | Enhanced abundance of CD8 + T cells with decreased MHC-II expression in APCs | ||||
C5a | Recruit neutrophils and monocytes from the circulation to the lung | C5a-C5aR1 axis is activated and promote immune dysfunction and pulmonary inflammation | Complement-dependent immunoinflammation | ||
C3a | Complement activation induces excessive T cell cytotoxicity | Complement activation creates an inflammatory milieu that drives differentiation of T cells with high immunopathogenic potential |
