. Author manuscript; available in PMC: 2024 Nov 1.

Published in final edited form as: Semin Immunol. 2023 Aug 29;70:101835. doi: 10.1016/j.smim.2023.101835

Table 3.

Transcriptional heterogeneity of lymph node blood endothelial cells.

Type of BEC	BEC subpopulations	Unique transcriptomic signature	Function	References
Capillary endothelial cells (CapEC)	Capillary endothelial cell type I (Cap-EC1)	Igfbp3⁺, Col4a1⁺, Col4a2⁺, Id1⁺, Id3⁺	(1) Express molecules that facilitate the maintenance of vascular tone and blood pressure. (2) Higher expression of Id1 and Id3 help control cell differentiation and senescence via inhibiting the DNA binding of basis helix-loop-helix proteins.	[97, 204]
	Capillary endothelial cell type II (Cap-EC2)	Erg1⁺, Cxcl1⁺, Sgk1⁺, Nr4a1⁺, Jun⁺, Junb⁺, Jund⁺, Fos⁺, Nfkbia⁺	CapEC2 transcriptome suggests that they are capable of responding to cytokines and other inflammatory mediators, possibly in response to disturbance in shear stress.	[97, 204]
	Interferon-stimulated gene-enriched CapEC (CapIfn EC)	Ifit1⁺, Ifit2⁺, Irf7⁺, Cxcl9⁺, Cxcl10⁺	CapIfn represents CapEC subset particularly responsive to IFN-signaling.	[97]
	Activated CapEC (CRP)	Angpt2⁺, Apln⁺, Esm1⁺, Pgf⁺, Nid2⁺, Kit⁺, Sox7⁺, Ets2⁺	(1) CRP represents a rare pluripotent EC subset, which acts as a precursor for other differentiated EC. (2) CRP EC possesses a gene signature indicative of activated capillaries that are capable of forming new blood vessels.	[97]
	Transitional phenotype EC (TrEC)	Chst2⁺, St3Gal6⁺, Fut7⁺	(1) Express genes signature indicative of transitory phenotype shared between the HEV and CapEC. (2) TrEC connects capEC to venous EC. (3) May help tether the lymphocytes to the vessel wall under shear stress and facilitate the recruitment of lymphocytes.	[97, 204]
Arterial endothelial cells	Arterial EC (ArtEC)	Cd31⁺, Gja4 (Connexin 40)⁺, Gja5(Connexin37)⁺, Bmx⁺, Sox17⁺, Gkn3⁺	Maintain blood flow and pressure in arteries.	[97, 204]
Venous endothelial cells	High endothelial venule (HEV)	Cd31⁺, PNAd⁺, Ccl21⁺, Chst4⁺, Glycam1⁺	(1) HEV produces CCL19 and CCL21 gradient and adhesion molecules required to chemoattract CCR7⁺ DCs and lymphocytes into the LN. (2) HEV vigorously responds to immune activation signals, thereby contributing to the structural change required for the LN expansion and accumulation of inflammatory cells.	[96, 97, 205]
Venous endothelial cells	Non-high endothelial cell venule (non-HEV)	Nr2f2⁺, Ackr1⁺, Sele⁺, Selp⁺, Vcam1⁺	Facilitate the rolling and crawling of circulating lymphocytes and myeloid cells via L- and P-selectin, ICAM1, and VCAM1 molecules.	[96, 97]