Changelog

This is the changelog for the ImmPrint collection, the curated data itself. It is versioned independently of the immprintr R package that delivers it. Each released collection snapshot is immutable; new curation ships as a new version.

0.2.0-alpha

Adds a regulatory role annotation, replaces many animal-only citations with human ones and extends cell type to multiple lineages.

  • New column regulatory_role, placed after the signalling tier (pathway_level) and before cell_type. It records each gene’s effect on its own pathway: none for a forward component or output, inhibitory for a negative regulator, activating for genuine positive feedback, and context_dependent where the sign varies.
  • Citations were reassessed to replace animal-only foundational references with verified human pathway-explicit primary sources wherever a clean one exists. 83 memberships had their PMID set revised; where no clean human primary exists the foundational reference is kept.
  • cell_type now records multiple lineages per membership where the biology warrants, ;-delimited (for example Epithelial; Fibroblast), and refinement rows that previously duplicated a gene across lineages are consolidated into a single multi-value row.
  • The inhibitory checkpoints PD1 and CTLA4 are stamped T cell across their receptor and transducer tiers, and IL7 is likewise restricted to T cell throughout, since its receptor is lymphoid-restricted and human IL7R loss of function spares B and NK cells. IL15 is restricted to T cell; NK cell, its responder lineages. IL15RA is removed, since the high-affinity chain is expressed by the trans-presenting myeloid or stromal cell rather than the responder, and ImmPrint records genes expressed by the responding cell. Cytolytic effectors are T cell; NK cell. 55 memberships had their cell type revised.
  • CD80 and CD86 are removed from IMMPRINT_CTLA4_SIGNALLING. They are the B7 ligands on the antigen-presenting cell rather than components of the T-cell signal, so they sit outside a signalling set on the same grounds costimulatory molecules are excluded from MHC class II.
  • TNFAIP3 (A20) and NFKBIA (IκBα) are added to IMMPRINT_TNF_SIGNALLING at the transducer tier with regulatory_role = inhibitory. Both are TNF-induced, but they enter as components rather than as induced outputs because each acts back on the cascade itself.
  • MCL1 is added to IMMPRINT_IL7_SIGNALLING at the effector tier, joining BCL2 as an IL-7 driven survival output. Both cite the same human primary, which shows IL-7 sustaining Bcl-2 and Mcl-1 through STAT5 in human T cells.
  • GZMB is removed from IMMPRINT_IL21_SIGNALLING. Cytotoxic granule effectors stay in IMMPRINT_CYTOLYTIC_ACTIVITY rather than being duplicated into the cytokine signalling sets that prime them.
  • FASLG is removed from IMMPRINT_CYTOLYTIC_ACTIVITY. It kills through the Fas death-receptor pathway rather than granule exocytosis, so it falls outside the granule-mediated scope of the set. The KLR recognition receptors are retained as the recognition step that precedes degranulation.
  • GATA3 is added to IMMPRINT_IL4_IL13_SIGNALLING.
  • CXCL8, CCL2 and IL6 are added to IMMPRINT_IL1_SIGNALLING, and S100A8 to IMMPRINT_IL17_SIGNALLING, all at the effector tier. Each is an inflammatory output induced through the named pathway in human cells.
  • CSF2 (GM-CSF) is added to IMMPRINT_IL2_SIGNALLING and IMMPRINT_IL12_SIGNALLING at the effector tier rather than to IMMPRINT_IL23_SIGNALLING. In human T helper cells GM-CSF is induced by IL-2 through STAT5 and promoted by the IL-12 driven Th1 axis while the IL-23 axis constrains it, reversing the expectation set by mouse pathogenic-Th17 models.
  • Two accidental duplicate rows are removed from IMMPRINT_IL17_SIGNALLING: CXCL8 and DEFB4A each held a pan row alongside a lineage-scoped row for the same gene. The pan rows are kept with their citations merged, restoring the rule that a gene appears once per set.
  • The column order is gene_set, gene_symbol, pathway_level, regulatory_role, cell_type, pmids, reference_gene_set. The collection now holds 44 gene sets and 720 memberships.

0.1.0-alpha

First public snapshot.

  • 44 gene sets, 724 gene set memberships.
  • Every membership carries at least one PubMed citation.
  • Each gene is placed in the three-tier Receptor, Transducer, Effector signalling hierarchy.
  • Cell type structure: a cell type-agnostic pan core per pathway, with effector refinements layered on for specific lineages (listed below).
  • MSigDB corroboration (Hallmark, Reactome, GO:BP) recorded per membership in reference_gene_set where applicable.
  • Antigen-receptor and inhibitory-checkpoint pathways (TCR, BCR, CTLA4, PD1) are restricted to their defining lineage and terminate at the transducer tier by design.

Cell type variant genes

The genes added beyond each pathway’s pan core, by responding lineage. TCR and BCR carry no pan core, so the genes shown there are the full lineage-restricted set.

IMMPRINT_BCR_SIGNALLING

  • B cell: CD79A, CD79B, LYN, SYK, BTK, BLNK, PLCG2, PIK3CD, PIK3R1, AKT1, CARD11, BCL10, MALT1, NFATC1, NFKB1, RELA, VAV1

IMMPRINT_IFNG_SIGNALLING

  • Monocyte/Macrophage: FCGR1A, IL12B, CYBB

IMMPRINT_IL10_SIGNALLING

  • Monocyte/Macrophage: CD163, TIMP1, NFIL3, FCGR3A, MERTK

IMMPRINT_IL17_SIGNALLING

  • Epithelial: DEFB4A, S100A7, CCL20, CXCL8, LCN2, CXCL1
  • Fibroblast: IL6, CXCL8, CSF3, CXCL1, CCL20

IMMPRINT_IL4_IL13_SIGNALLING

  • B cell: FCER2, IGHE, IGHG4, IL4I1
  • Epithelial: MUC5AC, CLCA1, POSTN, SERPINB2, CAPN14
  • Monocyte/Macrophage: MRC1, FCER2, CCL18, ALOX15, TGM2

IMMPRINT_IL6_SIGNALLING

  • T cell: IL21, BCL6, ICOS

IMMPRINT_TCR_SIGNALLING

  • T cell: CD3D, CD3E, CD3G, CD247, LCK, FYN, ZAP70, LAT, LCP2, PLCG1, ITK, PRKCQ, CARD11, BCL10, MALT1, NFATC1, NFKB1, RELA, VAV1

IMMPRINT_TGFB_SIGNALLING

  • B cell: IGHA1, IGHA2
  • Epithelial: SNAI1, VIM, SNAI2, CDH2, FN1
  • Fibroblast: ACTA2, FN1, COL1A1, COL3A1, POSTN, TAGLN
  • T cell: FOXP3, ITGAE

IMMPRINT_TNF_SIGNALLING

  • Endothelial: ICAM1, SELE, CX3CL1, F3
  • Fibroblast: MMP1, MMP3, MMP14
Note

The alpha label signals that the collection is still growing and that definitions and citations may change between alpha snapshots. Pin the version you use, and cite it (see Cite). The first non-alpha release will freeze a stable baseline.