INT221431

Context Info Confidence 0.40 First Reported 2007 Last Reported 2010 Negated 0 Speculated 0 Reported most in Body Documents 8 Total Number 8 Disease Relevance 9.92 Pain Relevance 1.98

growth (FOXP3) nucleus (FOXP3) intracellular (FOXP3) embryo development (FOXP3) protein complex (FOXP3) cytoplasm (FOXP3)

Anatomy Link Frequency regulatory T cells 1 FOXP3 (Homo sapiens)

Pain Link Frequency Relevance Heat Inflammation 131 98.16 tolerance 64 95.84 Inflammatory response 16 94.04 antagonist 14 89.44 cytokine 115 88.48 chemokine 15 73.44 rheumatoid arthritis 75 68.24 corticosteroid 48 67.28 Inflammatory mediators 3 64.88 cINOD 7 64.64

Disease Link Frequency Relevance Heat Immune Reconstitution Inflammatory Syndrome 124 99.48 Syndrome 29 99.32 Systemic Lupus Erythematosus 15 98.68 INFLAMMATION 136 98.16 Eosinophilia 6 97.68 Thrombocytopenia 5 97.00 Anaemia 1 96.28 Mycobacterial Infection 77 95.32 Acquired Immune Deficiency Syndrome Or Hiv Infection 139 95.20 Eczema 5 94.64

Sentences Mentioned In

Key:

Protein

Mutation

Event

Anatomy

Negation

Speculation

Pain term

Disease term

CD4+CD25high regulatory T cells from active but not inactive SLE patients were deficient in in vitro suppressive activity and had decreased Foxp3 mRNA and protein [132,133].

Negative_regulation (decreased) of Foxp3 in regulatory T cells associated with systemic lupus erythematosus

1) Confidence 0.40 Published 2008 Journal Pediatr Rheumatol Online J Section Body Doc Link PMC2633304 Disease Relevance 1.22 Pain Relevance 0.07

This 'paradoxical worsening' could also be attributable to additional presence of defective FOXP3+ gene among IRIS developers.

Negative_regulation (presence) of FOXP3 associated with immune reconstitution inflammatory syndrome

2) Confidence 0.35 Published 2007 Journal AIDS Res Ther Section Body Doc Link PMC2216023 Disease Relevance 1.07 Pain Relevance 0.41

This 'paradoxical worsening' could also be attributable to additional presence of defective FOXP3+ gene among IRIS developers.

Negative_regulation (defective) of FOXP3 associated with immune reconstitution inflammatory syndrome

3) Confidence 0.35 Published 2007 Journal AIDS Res Ther Section Body Doc Link PMC2216023 Disease Relevance 0.90 Pain Relevance 0.28

This 'paradoxical worsening' could also be attributable to additional presence of defective FOXP3+ gene among IRIS developers.

Negative_regulation (presence) of FOXP3 associated with immune reconstitution inflammatory syndrome

4) Confidence 0.35 Published 2007 Journal AIDS Res Ther Section Body Doc Link PMC2216023 Disease Relevance 0.90 Pain Relevance 0.28

This 'paradoxical worsening' could also be attributable to additional presence of defective FOXP3+ gene among IRIS developers.

Negative_regulation (defective) of FOXP3 associated with immune reconstitution inflammatory syndrome

5) Confidence 0.35 Published 2007 Journal AIDS Res Ther Section Body Doc Link PMC2216023 Disease Relevance 1.07 Pain Relevance 0.41

Baan and colleagues (2005) have found that monoclonal anti-CD25 antibodies (in this case, daclizumab) do, in fact, reduce FOXP3 messenger RNA levels in vitro.

Negative_regulation (reduce) of FOXP3 messenger RNA

6) Confidence 0.17 Published 2008 Journal Biologics : Targets & Therapy Section Body Doc Link PMC2721359 Disease Relevance 0.08 Pain Relevance 0.12

In humans, an X-linked genetic defect in Foxp3 is the underlying cause of a condition that presents with multiple autoimmune conditions, which is named the immuno-dysregulation, polyendocrinopathy, enteropathy (IPEX) syndrome69).

Negative_regulation (defect) of Foxp3 associated with enteropathy

7) Confidence 0.17 Published 2010 Journal Korean Journal of Pediatrics Section Body Doc Link PMC3012271 Disease Relevance 0.86 Pain Relevance 0.38

IPEX is secondary to mutations of the FOXP3 gene and a resultant deficiency of Treg cells.

Negative_regulation (deficiency) of FOXP3 gene associated with syndrome

8) Confidence 0.07 Published 2010 Journal Clin Mol Allergy Section Body Doc Link PMC2837605 Disease Relevance 3.83 Pain Relevance 0.04

General Comments

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