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Table 1 Pattern recognition receptors for SARS-CoV-2 infection

From: Innate immune recognition against SARS-CoV-2

Classification 

PRR

Ligands

Virus/host*

Experimental models

References

TLR

TLR2

?

–

Computational method with the dataset of BAL† from COVID-19 patients

[55]

E proteina

Virus

Mouse BMDM, Human PBMC

[56]

S proteina

Virus

Mouse BMDM

[57]

TLR3

? 

–

Genetic variant analysis in patients with life-threatening COVID-19b 

[21]

?

–

Calu-3/MRC-5 multicellular spheroids

[58]

TLR4

S proteina

Virus

Mouse peritoneal macrophages, mouse BMDM

[59]

S protein

Virus

Mouse peritoneal exudate macrophages, mouse RAW264.7 cells, human THP-1 cells

[60]

S protein

Virus

In silico study

[61]

TLR7

?

–

Genetic variant analysis in young men with severe COVID-19

[19]

?

–

Genetic variant analysis in patients with life-threatening COVID-19b

[20]

?

–

Calu-3/MRC-5 multicellular spheroids

[58]

RLR

MDA5

?

–

Calu-3 cells

[62,63,64,65,66]

(–)RNA

Virus

Calu-3 cells, RIG-I KO A549 cells

[67]

RIG-I

?

–

Calu-3 cellsc

[66]

RNA of SARS-CoV-2-infected Vero E6 cells

–

HEK293 cells

[68]

(+)gRNA

Virus

A549 cells, human primary bronchial, and alveolar epithelial cells (as a direct restraining factor)

[67]

CLR

DC-SIGN

L-SIGN

LSECtin

ASGR1

CLEC10A

S protein

Virus

Human PBMC-derived myeloid cells

[69]

NLR

NLRP3

?

–

Human monocytes derived from COVID-19 patients

[31, 70]

?

–

Human monocytes in lung tissues of COVID-19 patients

[70]

?

–

Human PBMC derived from COVID-19 patients

[70]

?

–

Human monocytes

[70, 71]

GU-rich RNA

Virus

Human macrophages

[72]

ORF3a

Virus

HEK293T cells, A549 cells

[73]

N proteind

Virus

Mouse BMDM, THP-1 cells, HEK293T cells, A549 cells

[74]

S protein

Virus

Human macrophages derived from COVID-19 patients

[75]

NOD1

?

–

Calu-3 cells

[62]

ALR

AIM2

Mitochondrial DNA?

Host

Human monocytes of COVID-19 patients

[31]

Other

cGAS

?

–

ACE2-expressing A549 cellse

[76]

DNA?

Host

ACE2-expressing A549 cells, HEK293T cells, HeLa cellse

[77]

Mitochondrial DNA

Host

Human endothelial cells in lung-on-chip model

[38]

Damaged DNA

Host

Human macrophages in skin lesions and lung tissues of COVID-19 patients

[38]

  1. *The origin of each ligand or possible ligand that activates PRRs. †BAL bronchoalveolar lavage. The involvement of PRRs and their ligands in SARS-CoV-2 infection is still controversial. In contrast to the supporting evidence regarding usage of some PRRs/ligands as above, there have been contradictory reports that do not support the involvement of some of those PRRs/ligands, although this might be caused by different cell types and/or experimental conditions that were used in each report: aTwo reports show viral E or S protein do not induce inflammatory response in some types of cells [56, 57]. bThere are genetic variant analysis data that do not support the involvement of TLR3 and TLR7 [78]. cAs for RIG-I, SARS-CoV-2-induced IFN responses are not affected by RIG-I deficiency in Calu-3 cells [62,63,64,65,66,67]. dSARS-CoV-2 N protein is reported to inhibit NLRP3-dependent inflammasome in THP-1 cells and human primary monocytes [79]. eDeficiency of STING does not affect types I and III IFN responses in Calu-3 cells during SARS-CoV-2 infection [64, 65]