Disease relevance of TH1L

• Different patterns of cytokine release are characteristic of certain subgroups of T helper cells, termed TH1 and TH2, the former mediating delayed-type hypersensitivity and the latter mediating IgE synthesis and eosinophilia [1].
• Experimental autoimmune encephalomyelitis (EAE) is a prototype autoimmune disease mediated by type 1 helper T (TH1) cells and under the control of regulatory cells [2].
• Ability of HIV to promote a TH1 to TH0 shift and to replicate preferentially in TH2 and TH0 cells [3].
• Murine TH1 but not TH2 cells are recruited through P- and E-selectin into inflamed tissues, where they induce delayed-type hypersensitivity reactions [4].
• Plasmacytoid dendritic cells activated by influenza virus and CD40L drive a potent TH1 polarization [5].

Psychiatry related information on TH1L

• They act as a negative regulator of activated T cells, control immunoglobulin production, contribute to the regulation of the TH1/TH2 balance, and occupy a central role in anti-viral defense mechanisms [6].
• Drug abuse may alter the change from the (CD4+)CD45RA+ to the (CD4+)CD45RA- phenotype selectively, which recovers in HIV-1+ methamphetamine abusers during treatment from baseline to 4-weeks, as manifested by improved IL-2 production in vitro. of TH1 and TH2 cytokines during progression to AIDS [7].

High impact information on TH1L

• TWEAK-/- mice developed oversized spleens with expanded memory and T helper 1 (TH1) subtype cells upon aging and mounted stronger innate and adaptive TH1-based responses against tumor challenge [8].
• Infection with intracellular bacteria triggers an immediate innate response requiring macrophages, neutrophils and natural killer cells, whereas subsequent activation of an adaptive response through development of T-helper subtype 1 cells (TH1) proceeds during persistent infection [9].
• Many pathological processes, including those causing allergies and autoimmune diseases, are associated with the presence of specialized subsets of T helper cells (TH1 and TH2) at the site of inflammation [10].
• Defective suppressor T cell function, perhaps related to TH1/TH2 imbalance, probably intervenes by amplifying the anti-beta-cell autoimmune response whatever its triggering mechanism [11].
• T helper 1 (TH1) cells mediate cellular immunity, whereas TH2 cells potentiate antiparasite and humoral immunity [12].

Chemical compound and disease context of TH1L

• We report the construction of a single adenovirus encoding human tyrosine hydroxylase 1 (hTH-1) under the negative control of the tetracycline-based gene regulatory system [13].
• The clinical effects of glatiramer acetate (GA), an approved therapy for multiple sclerosis, are thought to be largely mediated by a T-helper 1 (TH1) to T-helper 2 (TH2) shift of GA-reactive T-lymphocytes [14].
• TH1/TH2 cytokines and inflammatory cells in skin biopsy specimens from patients with chronic idiopathic urticaria: comparison with the allergen-induced late-phase cutaneous reaction [15].
• Before dehydration, > 90% of the iron in hTH1 had Mössbauer parameters typical for high-spin Fe(II) in a six-coordinate environment [isomer shift delta (1.8-77 K) = 1.26-1.24 mm s-1 and quadrupole splitting delta EQ = 2.68 mm s-1] [16].
• Full-length human tyrosine hydroxylase 1 (hTH1) and a truncated enzyme lacking the 150 N-terminal amino acids were expressed in Escherichia coli and purified either with or without (6 x histidine) N-terminal tags [16].

Biological context of TH1L

• Furthermore, we observed that TH1 inhibited cell cycle progression in TH1 stably transfected 7721 cells compared with mock cells, and flow cell cytometry analysis suggested that the TH1 stably transfected 7721 cells were G(0)/G(1) phase-arrested [17].
• In a two-hybrid screen of human fetal liver cDNA library, TH1 was detected as a new interaction partner of A-Raf [18].
• These results indicate that a switch from the TH1 to the TH2 cytokine phenotype does not occur during the progression of HIV disease [19].
• Interleukin-12 (IL-12) is a cytokine that promotes cell-mediated immunity to intracellular pathogens by inducing type 1 helper T cell (TH1) responses and interferon-gamma (IFN-gamma) production [20].
• Thus, Rac2 activates TH1-specific signaling and IFN-gamma gene expression [12].

Anatomical context of TH1L

• It is not known whether subsets of dendritic cells provide different cytokine microenvironments that determine the differentiation of either type-1 T helper (TH1) or TH2 cells [21].
• Thus, a negative feedback loop from the mature T helper cells may selectively inhibit prolonged TH1 or TH2 responses by regulating survival of the appropriate dendritic cell subset [21].
• TH1 and TH2 cytokine control of thyrocyte survival in thyroid autoimmunity [22].
• CONCLUSION--Whereas TH1-type immunity to trophoblast is associated with URA and may play a role in reproductive failure, TH2-type immunity may be a natural response to trophoblast contributing to successful pregnancy [23].
• Regulation of TH1- and TH2-type cytokine expression and action in atopic asthmatic sensitized airway smooth muscle [24].

Associations of TH1L with chemical compounds

• HBEC thus drive the effector end of a TH1-controlled feedback loop, which protects airway mucosal tissues at the potential lesional site in asthma from overwhelming CD4+ TH2 (and potentially TH1) responses following allergen exposure [25].
• In the presence of PGE2, TH1-like responses are suppressed and TH0-like responses are shifted toward a TH2-like pattern dominated by the production of IL-4 and IL-5 [26].
• The effect of serine 19 phosphorylation on serine 40 (44 in TH2) phosphorylation is stronger in TH2 than in TH1 [27].
• TH0, TH1, and TH2 T cell clones were stimulated in the presence and absence of the prostaglandin E1 (PGE1) analog misoprostol and PGE2 [26].
• Recently, it was reported that histamine induced IL-18 and that IL-18 might act as a coinducer of TH1 and TH2 cytokines [28].

Other interactions of TH1L

• The binding between A-Raf and TH1 was specific, as no binding between TH1 and B-Raf or c-Raf was observed, and the amino-terminal 162 amino acids in the A-Raf regulatory domain were found to be sufficient for this interaction [18].
• Sustained T-bet expression confers polarized human TH2 cells with TH1-like cytokine production and migratory capacities [29].
• The results show that both IFN-gamma producing (Th1-like) and IL-4 producing (Th2-like) T cells recognizing LPGAP are expanded after infection with L. donovani in humans [30].
• In addition, in activated T helper lymphocyte clones, it has been demonstrated that IFN-gamma (TH1-like cytokine) and IL-5 (TH2-like cytokine) are differentially regulated by the AC system [31].
• Induction of systemic TH1-like innate immunity in normal volunteers following subcutaneous but not intravenous administration of CPG 7909, a synthetic B-class CpG oligodeoxynucleotide TLR9 agonist [32].

Analytical, diagnostic and therapeutic context of TH1L

• Using confocal microscopy, we found that TH1 colocalizes with A-Raf, which confirms our former results [17].
• CONCLUSIONS: Immunotherapy with AS101 enhances TH1 function while interfering with the TH2 response [33].
• Our results indicate that intranodal vaccination with semimature DCs can prime strong, long-lasting CD4 T-cell responses with a TH1-type cytokine profile in cancer patients [34].
• These results suggest that G-CSF decreases IFN-gamma and increases IL-4 production in vitro and in vivo and likely modulates a balance between TH1 and TH2 cells, an effect that may be important in PBSC transplantation [35].
• The TH1/TH2 imbalance was more related to TH2 over-expression than to TH1 deficiency and persisted for at least 1 year under HAART [36].

References