Table 1.
Summary of pattern recognition proteins (PRPs) proinflammatory, anti-inflammatory and antiviral effects.
| Pattern recognition proteins (PRPs) | Proinflammatory effects | Anti-inflammatory effects | Effects on RNA viruses |
|---|---|---|---|
| Surfactant protein D (SP-D) | Trimer, monomer- CD91-CRT/OSCAR; enhance TNF-α and atherogenesis; overwhelmed inflammation | Dodecamer, fuzzy form-apoptotic cells/CD91-CRT; enhance phagocytosis; SP-D-SIRPα: anti-inflammatory | Anti-influenza through carbohydrate recognition domain-binding; virus aggregation/neutralization; hemagglutinin/neuraminidase activity (influenza) inhibition |
| Surfactant protein A (SP-A) | Abnormal clearance of apoptotic cells; Overwhelmed inflammation | SP-A-apoptotic cells/CRT-CD91; enhances phagocytosis and macrophage TGF-β | RNA virus (Influenza) agglutination and macrophage uptake; hemagglutinin inhibition |
| Mannose-binding lectin (MBL) | Overwhelmed inflammation; Abnormal macrophage uptake of apoptotic cells | MBL-apoptotic cells/CRT-CD91; enhance phagocytosis | RNA virus/apoptotic cell macrophage uptake |
| Complement component 1q (C1q) | Overwhelmed inflammation; Abnormal macrophage uptake of apoptotic cells | C1q-apoptotic cells/CRT-CD91; enhance phagocytosis | RNA virus/apoptotic cell macrophage uptake |
| Native C-reactive protein (nCRP) | Pentameric nCRP-FcγRI/FcγRIIa: increases inflammatory cytokine release; nCRP- FcγRIIb maintains a predominant anti-inflammatory effect | Pentameric nCRP bound to phosphorylcholine (PC) or lysoPC-apoptotic cells, C1q and factor H: enhance phagocytosis; nCRP-FcγRs: M2 response | Pentameric nCRP facilitates antimicrobial activity in pneumonia complicating COVID-19 infection |
| Non-native CRP (nnCRP) | Enhances inflammation and complement activation; induces atherogenesis; mostly proinflammatory | It binds atherogenic LDL, reduces foam cell formation and could also be atheroprotective | Very high CRP levels in COVID-19-associated hyperinflammation could promote nnCRP generation and inflammation |
| Monomeric CRP (mCRP) | Promotes chemotaxis; increases IL-8, MCP-1 and nitric oxide; induces ROS; mCRP-FcγRIII induce inflammation; promotes adhesion molecule expression, thrombosis and atherogenesis | Monomeric mCRP is mainly proinflammatory and not anti-inflammatory | Very high CRP levels in COVID-19-associated hyperinflammation could promote mCRP generation, inflammation, thrombosis and atherogenesis and plaque instability mediated by MMP1, 2 and 9 |
| Natural (innate) Immunoglobulin M (IgM) | Lack of innate IgM response allows cell necrosis and inflammation. Lung inflammation promotes apoptotic cell clearance | Non-inflammatory clearance of apoptotic cells; enhances virus and bacteria phagocytosis | Ancient antiviral weapon. IgM-enriched intravenous immunoglobulins (pentaglobin) will enhance antiviral protection against COVID-19 and apoptotic cell removal |
| Immune (adaptive) IgM | Lack of innate IgM response allows cell necrosis and inflammation | Non-inflammatory clearance of apoptotic cells; enhances virus and bacteria phagocytosis | Ancient antiviral weapon. IgM-enriched intravenous immunoglobulins (pentaglobin) will enhance antiviral protection against COVID-19 and apoptotic cell removal |
RNA, ribonucleic acid; CRT, calreticulin; OSCAR, osteoclast-associated receptor; SIRPα, signal inhibitory regulatory protein α; TGF-β, transforming growth factor-β; FcγR, Fcγ receptor; IL, interleukin; MCP-1, monocyte chemoattractant protein-1; ROS, reactive oxygen species.