Disease relevance of CCL22

• CCL22 also had the ability to chemoattract human Th2 cells and CEM cells in a pertussis toxin-sensitive manner [1].
• Selective induction of Th2-attracting chemokines CCL17 and CCL22 in human B cells by latent membrane protein 1 of Epstein-Barr virus [2].
• Finally, serum CCL22 levels were significantly elevated in infectious mononucleosis [2].
• CCL22 and CCL17 in rat radiation pneumonitis and in human idiopathic pulmonary fibrosis [3].
• On further analysis of bronchoalveolar lavage fluid from patients with idiopathic pulmonary fibrosis and sarcoidosis, elevated levels of CCL22, but not of CCL17, were observed in the idiopathic pulmonary fibrosis patients [3].

Psychiatry related information on CCL22

• However, since all abnormal ultrasound scans were found in children with a mitochondrial disorder, and no significant correlation with the MDC score was found, muscle ultrasound can be used complementary to this scoring system to facilitate the decision-making in pursuing further invasive diagnostics [4].
• This article presents one such effort, the Roberts' Triple ABCD Model. This model is an up-to-date and integrated conceptual framework that helps to provide the foundation for developing a unified standard of care for crisis and disaster mental health interventions [5].
• STCP smoking cessation efforts are targeted at specific populations that are at greater risk for developing cancer including youth, minority and ethnic groups, women, smokeless tobacco users, and heavy smokers [6].

High impact information on CCL22

• A protein associated with this activity was purified from the culture supernatant of an immortalized CD8(+) T cell clone and identified as the beta-chemokine macrophage-derived chemokine (MDC) [7].
• Blood-borne CD4(+) T cells that migrate in response to CCL1 and CCL22 exhibit a reduced alloproliferative response, dependent on the increased frequency of Treg cells in the migrated population [8].
• Importantly, mature dendritic cells preferentially attract Treg cells among circulating CD4(+) T cells, by secretion of CCR4 ligands CCL17 and CCL22 [8].
• ABCD-1 mRNA is found in highest quantities in activated splenic B lymphocytes and dendritic cells [9].
• Recombinant ABCD-1 revealed a concentration-dependent and specific migration of activated splenic T lymphoblasts in chemotaxis assays [9].

Chemical compound and disease context of CCL22

• Cocaine, in synergy with HIV peptides, also up-regulates DC-SIGN gene expression by MDC [10].
• Here we examined the presence of PDC together with myeloid dendritic cells (MDC) in the nasal epithelia of healthy individuals, of asymptomatic patients with chronic nasal allergy, of patients undergoing steroid therapy, and of patients with infectious rhinitis or rhinosinusitis [11].
• CONCLUSIONS: ABCD, like other lipid-based and liposomal formulations of amphotericin B, has been designed to deliver the active drug to the target site, while reducing renal toxicity [12].
• Even at daily doses as high as 6 mg/kg, and mean and median cumulative doses of 4.0 g and 2.4 g, respectively, ABCD had little renal toxicity: the mean change in serum level of creatinine from baseline to final value was -0.02 mg/dL [13].
• Amphotericin B colloidal dispersion (ABCD), a novel formulation of amphotericin B and cholesteryl sulfate in a 1:1 ratio, was developed to reduce the toxicity of amphotericin B yet retain its antifungal efficacy [13].

Biological context of CCL22

• Several other chemokines in addition to CXCL10 were able to increase CCL22-mediated chemotaxis [14].
• In this regard, CCL22 stimulates phosphatidylinositol-3 kinase-independent phosphorylation of the novel delta isoform of PKC at threonine 505, situated within its activation loop--an event closely associated with increased catalytic activity [15].
• In contrast, expression of Th2-associated chemokines does not strictly correlate with the Th2-promoting DC phenotype, except for CCL22/MDC, which is preferentially expressed by Th2-promoting DC [16].
• To explore this relationship in greater detail, we have more precisely localized the MDC gene to chromosome 16q13, the same position reported for the TARC gene [17].
• In addition, the genes for MDC and TARC are encoded by human chromosome 16 [17].

Anatomical context of CCL22

• The third wave, which occurs after 24 to 48 hours, when DCs have reached the lymphoid organs, includes CCL19, CCL22, and CXCL13, which attract naive T and B lymphocytes [18].
• Dendritic cells as a major source of macrophage-derived chemokine/CCL22 in vitro and in vivo [19].
• Migration of Th1/CCR5+ and Th2/CCR4+ effector lymphocytes toward CCR5 (CCL5, CCL3L1) and CCR4 (CCL22) ligands is affected by cleavage [20].
• CCL17 and CCL22 attenuate CCL5-induced mast cell migration [21].
• CXCL12 can be secreted by endothelial cells and is present in atherosclerotic plaques, whereas CCL17 and CCL22 are secreted by monocytes and macrophages [22].

Associations of CCL22 with chemical compounds

• Although both CCL17 and CCL22 caused mobilization of intracellular calcium, none of them induced migration or histamine release [21].
• In contrast, inhibition of the B7:CD28 pathway using a CTLA-4-Ig fusion protein completely inhibited diesel-dependent increase of allergen-induced MDC production [23].
• We conclude that minimal NH2-terminal truncation of MDC differentially affects its various immunologic functions [24].
• However, CCL22 is much more powerful than CCL17 in the induction of rapid integrin-dependent T cell adhesion on VCAM-1 under conditions of physiological flow [25].
• Adenosine diphosphate strongly potentiates the ability of the chemokines MDC, TARC, and SDF-1 to stimulate platelet function [26].

Physical interactions of CCL22

• The chemokine receptor CCR4 binds MDC with high affinity and also responds by calcium flux and chemotaxis [27].
• A chemokine binding assay on whole cells was developed using biotinylated synthetic CCL22 as a model ligand [28].

Regulatory relationships of CCL22

• Macrophage-derived chemokine induces human eosinophil chemotaxis in a CC chemokine receptor 3- and CC chemokine receptor 4-independent manner [29].
• Finally, CCL22 was able to trigger actin polymerisation in peripheral CD4+ T-cells expressing CCR4 [30].
• CD40 ligation of PB cells induced the mRNA expression of both CCL22 and CCL17 [31].
• IFN-gamma also suppressed the constitutive expression of MDC in mature macrophages and dendritic cells [32].
• Here we demonstrate that MDC inhibits the replication of CCR5-dependent (R5) HIV-1(BaL) in monocyte-derived macrophages (MDM), but not in T cell blasts, although with variable potency depending on donor variability [33].

Other interactions of CCL22

• Intracellular staining confirms that CD3+CD4+ T cells are the source of the prototype HIV-1-inhibiting chemokines CCL22 and CCL4 [34].
• The results reveal a striking selectivity for stromal cell-derived factor-1alpha (CXCL12) and macrophage-derived chemokine (CCL22) [35].
• Also, CCR4 is internalized between 5 and 45 min but reappears in the membranes after 60 min of stimulation with MDC [36].
• However, MDC reactivity was consistently localized to the outer wall of Hassal's corpuscles, whereas ELC reactivity was often found in cells surrounding medullary vessels, but not in Hassal's corpuscles [37].
• The median serum levels of MDC (3131 vs. 2394 pg/ml; p = 0.031) and EOX (80 vs. 61 pg/ml; p = 0.046) were also higher in children with moderate as compared with mild AD [38].

Analytical, diagnostic and therapeutic context of CCL22

• Although MDC can act by means of CCR4, RT-PCR analysis failed to reveal CCR4 mRNA in eosinophils [29].
• The serum concentrations of TARC, MDC, eotaxin and IgE were measured with the use of enzyme-linked immunosorbent assay kits [39].
• RESULTS: Higher gene expression of MDC in lung cancer was significantly correlated with longer disease-free survival time and lower risk of recurrence after tumor resection [40].
• Levels of TARC, MDC, and MIG were significantly decreased after treatment when the skin lesions disappeared in these patients [41].
• Immunohistochemistry shows that MDC, fractalkine, and TARC are expressed by a subset of macrophages within regions of plaques that contain plaque microvessels [42].

References