A case developing minimal change disease during the course of IgG4-related disease.

We describe a 66-year-old male with immunoglobulin G4-related disease (IgG4-RD) presenting with minimal change disease (MCD). Three years prior to this admission, the patient had been diagnosed with IgG4-RD. The development of sudden massive proteinuria (4+; 16.

Efficacy of coronary artery screening tests and intervention in hemodialysis patients.

Although cardiovascular disease (CVD) is an important cause of death in patients on hemodialysis, evidence of a beneficial effect of percutaneous intervention (PCI) on stable heart disease is scarce. We investigated the cardiovascular outcomes of hemodialysis patients under our policy of encouraging coronary artery screening tests to the extent possible. A total of 147 hemodialysis patients have been treated in our clinic so far.

Ag and IL-2 immune complexes efficiently expand Ag-specific Treg cells that migrate in response to chemokines and reduce localized immune responses.

An intravenous administration of a high-dose antigen (Ag) can induce immune tolerance and suppress the immune response, but the mechanism remains unclear. We recently proved that a combined i.v.

Situs inversus and cystic kidney disease: Two adult patients with this Heterogeneous syndrome.

Background: Situs inversus is a rare complication of cystic kidney diseases. Only three genes, INVS (NPHP2), NPHP3 and PKD2 have been proved to be responsible for some cases, while the responsible genes in many others are still unknown.

Case Reports: Here we report two male patients with situs inversus combined with cystic kidney disease without any family history of polycystic kidney disease.

TNF optimally activatives regulatory T cells by inducing TNF receptor superfamily members TNFR2, 4-1BB and OX40.

TNF is a pleiotropic cytokine with intriguing biphasic pro-inflammatory and anti-inflammatory effects. Our previous studies demonstrated that TNF up-regulated FoxP3 expression and activated and expanded CD4+ FoxP3+ regulatory T cells (Tregs) via TNFR2. Furthermore, TNFR2-expressing Tregs exhibited maximal suppressive activity.

Expression of costimulatory TNFR2 induces resistance of CD4+FoxP3- conventional T cells to suppression by CD4+FoxP3+ regulatory T cells.

Our previous study showed that TNFR2 is preferentially expressed by CD4(+)FoxP3(+) regulatory T cells (Tregs), and expression of this receptor identified maximally suppressive Tregs. TNFR2 is also expressed by a small fraction of CD4(+)FoxP3(-) conventional T cells (Tconvs) in normal mice, and its expression is upregulated by T cell activation. This raises questions about the role of TNFR2 signaling in the function of Tconv cells.

Co-expression of TNFR2 and CD25 identifies more of the functional CD4+FOXP3+ regulatory T cells in human peripheral blood.

Previously, we found that co-expression of CD25 and TNFR2 identified the most suppressive subset of mouse Treg. In this study, we report that human peripheral blood (PB) FOXP3(+) cells present in CD25(high), CD25(low) and even CD25(-) subsets of CD4(+) cells expressed high levels of TNFR2. Consequently, TNFR2-expressing CD4(+)CD25(+) Treg included all of the FOXP3(+) cells present in the CD4(+)CD25(high) subset as well as a substantial proportion of the FOXP3(+) cells present in the CD4(+)CD25(low) subset.

A case of immunoglobulin G4-related chronic sclerosing sialadenitis and dacryoadenitis associated with tuberculosis.

We describe a 64-year-old woman with chronic sclerosing sialadenitis and dacryoadenitis, which developed during treatment for cervical lymph node tuberculosis. Anti-tuberculosis treatment did not improve the swelling in the lacrimal and submandibular glands, and a biopsy specimen of the lacrimal gland showed inflammation, with abundant lymphoid follicles with fibrosis and granuloma without caseous necrosis. Immunohistological examination of a repeat biopsy specimen showed abundant immunoglobulin (Ig) G4-positive plasma cell infiltration.

Systemic capillary leak syndrome associated with compartment syndrome.

Systemic capillary leak syndrome is characterized by recurrent hypovolemic shock attributable to increased systemic capillary leakage. A 26-year-old woman was admitted because of recurrent episodes of hypovolemic shock. Hemoconcentration, hypoalbuminemia, and monoclonal gammopathy were observed.