Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Lack of interferon-gamma production despite the presence of interleukin-18 during cutaneous wound healing.

Molecular medicine (Cambridge, Mass.) - 1 Dec 2000

Kämpfer H, Paulukat J, Mühl H, Wetzler C, Pfeilschifter J, Frank S

Abstract excerpt

BACKGROUND: Recently, we have reported a rapid and strong induction of interleukin-18 (IL-18) upon cutaneous injury in mice. In this paper, we investigated a possible role of IL-18 in triggering interferon-gamma (IFN-gamma) production at the wound site. MATERIALS AND METHODS: Expression of IFN-gamma during cutaneous wound healing was analyzed by RNase protection assay, Western blot, ELISA, and immunohistochemical...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Diabetes Mellitus, Experimental
Share to Interferon-gamma

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Interleukin-18

Share to Lymphocytes

Share to Mice, Inbred DBA

Share to Ribonucleases

Share to Tissue Distribution

Share to Wound Healing

Source

Open in PubMed Open full text

Identifiers

PMID: 11474118
PMCID: PMC1949929

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Lack of interferon-gamma production despite the presence of interleukin-18 during cutaneous wound healing.PMID 11474118Read ↗

Burn wound γδ T-cells support a Th2 and Th17 immune response.Semantic proximity Read ↗

Inflammation in wound repair: molecular and cellular mechanisms.Semantic proximity Read ↗

Ameliorated course of glucose-6-phosphate isomerase (G6PI)-induced arthritis in IFN-γ receptor knockout mice exposes an arthritis-promoting role of IFN-γ.Semantic proximity Read ↗

Genetically resistant mice lacking IL-18 gene develop Th1 response and control cutaneous Leishmania major infection.Semantic proximity Read ↗

Incisional wound healing in transforming growth factor‐β1 null miceSemantic proximity Read ↗

A role for endogenous transforming growth factor beta 1 in Langerhans cell biology: the skin of transforming growth factor beta 1 null mice is devoid of epidermal Langerhans cells.Semantic proximity Read ↗

Interferon-gamma regulates susceptibility to collagen-induced arthritis through suppression of interleukin-17.Semantic proximity Read ↗

Genetic absence of gamma-interferon delays but does not prevent diabetes in NOD mice.Semantic proximity Read ↗

IL-10 overexpression decreases inflammatory mediators and promotes regenerative healing in an adult model of scar formation.Semantic proximity Read ↗

Delayed wound healing in the absence of intercellular adhesion molecule-1 or L-selectin expression.Semantic proximity Read ↗

Injury-induced suppression of effector T cell immunity requires CD1d-positive APCs and CD1d-restricted NKT cells.Semantic proximity Read ↗

Differences in wound healing in mice with deficiency of IL-6 versus IL-6 receptor.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.