Table 1 Inhibitory coreceptor expression on various non-T cell populations.

DCs

Upregulated in tumors, inflammation, sepsis

Reduces antigen presentation, cytokine production and survival; inhibits NFκB; promotes apoptosis; and decreases CD8⁺ T cell activation

SHP2-dependent NFκB inhibition, suppresses DC maturation, LPS-induced apoptosis, impairs bacterial clearance and interferes with CD40/MAPK1; ↑ IL10, ↓ IL12p70

^{23,24,25,26,27,28}

Mast cells

Detected in mastocytosis

Regulates proliferation and contributes to immune suppression and resistance to anti-PD1 therapy

SHP1/2 phosphorylation upon PDL1 binding (LAD2 cells), and cell–cell contact induces tolerogenic DCs via IDO

^31,32,33

B cells

Upregulated upon activation

Inhibits BCR signaling and activation, supports memory B cell and antibody responses and suppresses antitumor immunity

SHP2 recruitment and dephosphorylation of PI3K and Erk1/2, also supports cMyc-driven class switch, antibody production and memory formation; ↑ IL10

^{34,35,36,37,38,39}

ILCs

Expressed ILC1, ILC2, ILC3 and progenitors

Suppresses ILC function, limits cytokine production and affects gut and tumor immunity

ILC1: PD1 suppresses IFNγ, GzmB, and tumor lactate upregulates PD1 and rewires metabolism

ILC2: PD1 suppresses CCL5 and reduces DC recruitment

ILC3: PD1 loss ↓ IL22 (gut homeostasis)

^{49,50,51,52,53,54,55,56}

Macrophages

Upregulated in sepsis, tumors, spinal cord injury

Suppresses phagocytosis, shifts polarization to M2 (immunosuppressive) and reduces inflammation in sepsis

Inhibits STAT1 (↓M1), promotes STAT6 (↑M2); impairs phagocytosis; suppresses glycolysis and antigen presentation; PD1–PDL1 blockade restores function

^40,48

DCs

Expressed in monocyte-derived DCs (upregulated with TLR ligands)

Modulates maturation, cytokine production and antigen presentation

CTLA4 litigation ↓ IL12, ↑ IL10; siRNA knockdown enhances T cell stimulation; vesicle secretion of CTLA4 reduces B7 on neighboring DCs, limiting T cell priming

^75,76,77,78

Monocytes

Constitutively expressed on CD14⁺ cells

Limits activation marker expression and proliferation

Anti-CTLA4 antibody blocks IFNγ-induced upregulation of CD86 and HLA-DR

⁷⁴

B cells

Expressed upon IL4 activation and in B-1a cells

Inhibits class switch recombination and regulates B-1a cell tolerance

Suppresses germline Cε and Cγ1 gene transcription and inhibits transcription factors needed for isotype switching; absence in B-1a → GC and T_FH skewing, self-reactivity

^80,81

DCs

Expressed in BMDCs and highly in pDCs (constitutively, even without stimulation)

Regulates cytokine production and T cell priming

Lag3-deficient DCs →

↑ TNF (baseline);

↓ fatty acid oxidation,

↑ glycolysis;

pDCs: Lag3 limits expansion under CpG but not MHCII or TLR9 expression

^102,104

B cells

Expressed in activated B cells (T cell dependent) and IL10⁺ CD138⁺ plasma cells

Immunosuppressive and limits memory T cell formation after infection

Induced by T cell-derived factors, Lag3⁺ plasma cells express IL10 and maintain quiescence and suppress CD8⁺ T cell memory responses post-infection

^105,106

Microglia

Expressed and upregulated by IFNγ/STAT1 in mice and expressed in human microglia

Regulates inflammatory activity and may influence neurogenesis and behavior

Knockdown increases inducible nitric oxide synthetase expression, blocking Lag3 has antidepressant-like effects and increases neurogenesis and

reduced Lag3⁺ microglia in suicidal bipolar disorder

^{107,108,109,110}

DCs

Highly expressed on cDC1s and pDCs

Limits inflammation, cross-presentation and cytokine output and inhibits antitumor immunity

Binds PtdSer → phagocytosis and cross-presentation; binds HMGB1 → suppresses TLR responses; limits CXCL9 and inflammasome activity (IL1β, IL18)

^{117,118,119,120,121,123}

Macrophages/TAMs

Constitutively expressed in monocytes/macrophages and upregulated in tumors

Suppresses inflammatory cytokine production and promotes tumor progression (for example, HCC)

Tim3 knockdown →

↑ IL12, ↓ TAM activation;

Gal9 binding → enhances IL1β in M. tuberculosis infection and modulates TLR signaling

^{125,126,127,128,129,130}

Microglia

Basal expression, upregulated by LPS and hypoxia

Modulates neuroinflammation, phagocytosis and polarization and affects brain injury outcomes

↑ TGFβ, IL1β production;

knockdown → ↑ M2 polarization, ↓ infarct size/neutrophils; overexpression reverses neuroprotection in HIF1α-deficient models

^131,132

Macrophages

Elevated in M2-type macrophages (for example, in acute myeloid leukemia)

Maintains immunosuppressive M2 phenotype and inhibits phagocytosis

TIGIT blockade → repolarization to M1, ↑ CD226, ↑ CD47-mediated phagocytosis

¹⁴⁴

B cells

Expressed especially in Tim1⁺ and memory B cell subsets

Promotes IL10 production and immune tolerance, regulates T_FH cells and suppresses T cell responses

B cell TIGIT interacts with CD155⁺ T_FH → inhibits T_FH proliferation; TIGIT/Tim1⁺ B cells suppress inflammation; deficiency leads to autoimmunity

^145,147,148