Onychomycosis of the Middle Finger of a Japanese Judo Athlete due to Trichophyton tonsurans

We present a 17-year-old Japanese male high school student, who had applied steroid ointment for atopic dermatitis, with fingernail onychomycosis due to Trichophyton tonsurans. He was found positive for T. tonsurans infection based on hairbrush culture performed due to an epidemic of T. tonsurans infection in his judo club. The hairbrush culture method is very important in screening for this infection, and dermatologists should examine the entire body of athletes who are found positive using this method. For the diagnosis of T. tonsurans infection, other than the skin and hair, the nails should also be checked by dermoscopy because the fingernail may be the origin of this fungus.

False-positive serology following intravenous immunoglobulin and plasma exchange through transfusion of fresh frozen plasma in a patient with pemphigus vulgaris.

Intravenous immunoglobulin therapy and plasma exchange through transfusion of fresh frozen plasma are therapeutic options for patients with refractory pemphigus vulgaris. Passive acquisition of various clinically important antibodies through these therapies can occur, leading to false serology and negatively affecting patients' clinical care. It is recommended that dermatologists recognize the possibility of these phenomena and interpret them appropriately. Here, we report false-positive serology following intravenous immunoglobulin therapy and plasma exchange through transfusion of fresh frozen plasma in a patient with refractory pemphigus vulgaris. We also discuss the measure for misinterpretation and unnecessary clinical intervention.

Monocyte chemoattractant protein-1 contributes to gut homeostasis and intestinal inflammation by composition of IL-10-producing regulatory macrophage subset.

Lamina propria macrophages (LPMs) spontaneously produce large amounts of anti-inflammatory IL-10 and play a central role in regulation of immune responses against commensal bacteria. MCP-1 is a chemokine that plays an important role in recruitment of monocytes and macrophages to inflamed tissues. We demonstrated that, in addition to IL-10, LPMs produced large amounts of MCP-1, even in a steady state. MCP-1 deficiency caused impaired IL-10 production by LPMs and led to exacerbation of dextran sulfate sodium-induced acute colitis. As an explanation of this impaired IL-10 production by LPMs, we found that LPMs could be separated into two subsets with distinct side-scattered properties, namely LPM1 (CD11b(+)F4/80(+)CD11c(-)SSC(hi)) and LPM2 (CD11b(+)F4/80(+)CD11c(-)SSC(lo)). Unlike LPM1, the LPM2 subset migrated in response to MCP-1 and produced a larger amount of IL-10 in response to commensal bacteria. LPMs isolated from MCP-1-deficient mice produced less IL-10 as a consequence of the lack of the MCP-1-dependent LPM2 population. This imbalanced composition in LPM population may be involved in the susceptibility to DSS-induced colitis in MCP-1-deficient mice. Our results suggest that endogenous MCP-1 contributes to the composition of resident LPM subsets in the intestine. Moreover, MCP-1-dependent LPM2 subset may play an important role in maintenance of gut homeostasis in the steady state, and in the termination of excess inflammatory responses in the intestine, by producing IL-10.

TL1A produced by lamina propria macrophages induces Th1 and Th17 immune responses in cooperation with IL-23 in patients with Crohn's disease.

BACKGROUND: Tumor necrosis factor (TNF)-like protein 1A (TL1A) is a member of the TNF superfamily and contributes to the pathogenesis of Crohn's disease (CD) by stimulating T-helper (Th) 1 cells. In addition to Th1, recent studies have focused on the role of Th17 cells in the pathogenesis of CD. Here we tried to clarify the role of TL1A in Th1 and Th17 immunity in CD. METHODS: TL1A expression was assessed by quantitative reverse-transcription polymerase chain reaction (RT-PCR) in lamina propria (LP) macrophages (LP-M phi s) from normal controls (NC) and patients with CD or ulcerative colitis (UC). Purified LP CD4(+) T cells were stimulated with TL1A and/or IL-23 and interferon gamma (IFN-gamma) and interleukin (IL)-17 levels were analyzed. We also examined the effect of TL1A on naïve CD4(+) T-cell differentiation. RESULTS: We found that LP-M phi s are a major producer of TL1A. TL1A expression was markedly enhanced in LP-M phi s from CD patients compared with NC or UC patients. IL-23, in addition to TL1A, was induced in LP-M phi s by commensal bacteria stimulation. TL1A and IL-23 synergistically promoted the production of IFN-gamma and IL-17 by LP T cells, while TL1A alone did not induce cytokine production. Furthermore, TL1A promoted Th17 differentiation from naïve T cells by LP-M phi s; however, IL-23 did not show any synergistic effects on Th17 differentiation. CONCLUSIONS: TL1A expressed in LP-M phi s might play an important role in the pathogenesis of CD by inducing Th1 and Th17 immunity. IL-23 differentially regulated these functions of TL1A on memory and naïve T cells.

Human CD14+ macrophages in intestinal lamina propria exhibit potent antigen-presenting ability.

Intestinal APCs are considered critical in maintaining the balance between the response against harmful pathogens and the induction of tolerance to commensal bacteria and food Ags. Recently, several studies indicated the presence of gut-specific APC subsets, which possess both macrophage and dendritic cell (DC) markers. These unique APC subsets play important roles in gut immunity, especially for immune regulation against commensal bacteria. Herein, we examined a unique macrophage subset, which coexpressed the macrophage (Mphi) marker CD14 and the DC marker CD209 in human intestinal lamina propria (LP). The LP Mphi subset in both normal control subjects or Crohn's disease (CD) patients induced proliferation of naive CD4(+) T cells as well as monocyte-derived DCs, and it expressed retinoic acid synthetic enzyme retinaldehyde dehydrogenase 2 and retinol dehydrogenase 10, which induced expression of gut homing receptors on T cells in a retinoic acid-dependent manner. Moreover, the LP Mphi subset strongly evoked differentiation of Th1 cells and slightly induced Th17 cells in both normal control subjects and CD patients; the inducing potential was highest in CD patients. In CD patients, Th17, but not Th1, induction by the LP Mphi subset was enhanced in the presence of commensal bacteria Ags. This enhancement was not observed in normal control subjects. The Th17 induction by the LP Mphi subset was inhibited by neutralization of IL-6 and IL-1beta, but it was enhanced by blockade of retinoic acid signaling. These observations highlight a role for LP Mphi in the enhanced Th1, and potentially in Th17 differentiation, at the inflammatory site of inflammatory bowel diseases.