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. 2019 May 10;317(1):H124–H140. doi: 10.1152/ajpheart.00028.2019

Table 1.

Genes associated with T-cell immune responses in HF

Experimental Animal Models Disease Model Phenotype
Ischemic HF
I/R Acute Chronic Nonischemic HF Experimental autoimmunity References
Ccr2−/− or Ab depletion Protected (69)
Ccr5 −/− More damage (18)
Cd28 −/− More damage (107)
Cd4−/−, Ab depletion, MhcII−/− Protected More damage Protected (30, 44, 56)
Cxcr3 −/− Similar to WT Protected (64, 78)
Cxcl10−/− Protected (10)
Cd11c−/− or Ab depletion More damage Protected (37, 95)
Icam1 −/− Protected (76)
Ifng−/−, Ifngr−/− Protected Protected/more damage (2022, 28)
Il17a−/−, Il17ra−/− Protected (5, 99)
NOD DQ8+ More damage (51)
OTII Protected (44)
Pdcd1 (PD-1)−/− More damage (89)
Cd274 (PD-L1/2)−/− More damage (26, 89)
Rag2 −/− Protected (44)
Rorc −/− Protected (100)
Tbx21 −/− More damage (73)
Tcra −/− Protected (44, 61)
Treg DTR or Ab depletion Protected More damage Protected (7, 30, 56)

A protected phenotype frequently shows low inflammatory responses, which usually lead to a reduction of adverse cardiac remodeling. In contrast, a “more damage” phenotype is based on an increase in T-cell immune responses that mainly contributes to cardiac fibrosis and therefore to dilated cardiomyopathy. I/R, ischemic-reperfusion; Ab, antibody; HF, heart failure; WT, wild type.