. 2021 Feb 3;43(1):45–64. doi: 10.1007/s00281-021-00842-3

Table 1.

Features and risk factors of myasthenia gravis (MG) subtypes with anti-acetylcholine receptor (AChR) autoantibodies, comprising early-onset MG (EOMG), late-onset MG (LOMG) and thymoma-associated MG (TAMG) [82, 174–180]. Onset-ages may be subject to revision. EOMG and LOMG may prove to overlap, and the cut-off age(s) to differ between the sexes

MG type	Autoantigen targets	Onset-age (years)	M:F ratio	Genetic risk factors in Caucasians	Thymic pathology	AIRE⁺ mTECs	Myoid cells
EOMG	AChR	<50–60	1:3	MHC class I >II^a (CHRNA1^b) PTPN22 (CTLA4^low) (TNIP1)	Ectopic germinal centres	Normal number	Normal number
LOMG	AChR ± titin cytokines RYR1/2	>50–60	2:1	MHC class II >I^a TNFRS11A (PTPN22) (CTLA4^low	Atrophy	Reduced	Reduced
TAMG	AChR ± titin cytokines RYR1/2	Any (median age ~50)	1:1	None established (CTLA4^high)	Thymic epithelial neoplasm	Absent	Absent

CHRNA1 AChR a-subunit gene [82], PTPN22 protein tyrosine phosphatase, non-receptor-type, 22, CTLA4 cytotoxic T lymphocyte-associated 4: the unique CTLA4 high-expresser risk genotype in TAMG suggests a role of CTLA4 in central tolerance failure [176], TNIP1 TNFAIP3-interactin protein 1, TNFRS11A TNF receptor superfamily, member 11A (RANK), RYR1/2 ryanodine receptors 1 and 2

^aAssociations awaiting confirmation [174–177, 179, 180] are given in brackets; the HLA-DQA1*05:1 gene is predisposing in EOMG and protective in LOMG [177, 180]

^bCytokines (type I interferons; IL12)