Comparison of Demographic and Clinical Characteristics of Hispanic and Asian Chronic Hepatitis B Patients in Southern California.

Objectives: There are few data regarding the clinical and serologic features of chronic hepatitis B (CHB) infection among Hispanics in the United States. The aims of this study were to compare and contrast clinical characteristics of Hispanic and Asian CHB patients.

Methods: Demographic, clinical, and laboratory data were collected from Hispanic and Asian CHB patients seen between January 2013 and May 2014 at Los Angeles County Hepatitis Clinic.

Treatment Outcomes With First-line Therapies With Entecavir and Tenofovir in Treatment-Naive Chronic Hepatitis B Patients in a Routine Clinical Practice.

Background: Given their high efficacy, entecavir (ETV) and tenofovir (TDF), are the recommended first-line therapies for chronic hepatitis B, but it is not clear whether the efficacy reported from pivotal trials is similar to the outcomes seen in routine practice.

Goals: Our goal was to examine the treatment outcomes of antiviral therapy in such setting.

Patients And Methods: We conducted a retrospective study of 557 consecutive treatment-naive patients who started either ETV (n=443) or TDF (n=114) at 3 US liver clinics between January 2005 and 2012.

Suppression of an established immune response by UVA--a critical role for mast cells.

Exposing experimental animals or human volunteers to UVA II (320-340 nm) radiation after immunization suppresses immunologic memory and the elicitation of delayed-in-time hypersensitivity reactions. Previous studies indicated that the mechanisms underlying UVA-induced immune suppression are similar to those described for UVB-induced immune suppression, i.e.

Cis-urocanic acid, a sunlight-induced immunosuppressive factor, activates immune suppression via the 5-HT2A receptor.

Exposure to UV radiation induces skin cancer and suppresses the immune response. To induce immune suppression, the electromagnetic energy of UV radiation must be absorbed by an epidermal photoreceptor and converted into a biologically recognizable signal. Two photoreceptors have been recognized: DNA and trans-urocanic acid (UCA).

A role for inflammatory mediators in the induction of immunoregulatory B cells.

UV exposure suppresses the immune response to a variety of microbial, fungal, and viral Ags. In addition, UV radiation is a complete carcinogen and the immune suppression induced by UV radiation is a major risk factor for skin cancer induction. In this study, we examined the mechanisms underlying the induction of immune suppression and tolerance induction by UV radiation.

Platelet-activating factor is crucial in psoralen and ultraviolet A-induced immune suppression, inflammation, and apoptosis.

Psoralen plus UVA (PUVA) is used as a very effective treatment modality for various diseases, including psoriasis and cutaneous T-cell lymphoma. PUVA-induced immune suppression and/or apoptosis are thought to be responsible for the therapeutic action. However, the molecular mechanisms by which PUVA acts are not well understood.

Inverse relationship between increased apoptosis and decreased skin cancer in UV-irradiated CD1d-/- mice.

We previously demonstrated that CD1d knockout mice were resistant to ultraviolet (UV)-induced immunosuppression. Because immune suppression is a critical factor in the development of UV-induced skin cancers, we investigated the response of wild type (WT) and CD1d-/- mice to UV carcinogenesis. We found that although 100% of WT mice developed skin tumors after 45 weeks of UV irradiation, only 60% of CD1d-/- mice developed skin tumors.

Resistance of CD1d-/- mice to ultraviolet-induced skin cancer is associated with increased apoptosis.

Inhibition of p53-induced epidermal apoptosis, generation of p53 mutations, and suppressor T cells are the critical events responsible for the induction and development of UV-induced skin cancers. Recently, we demonstrated that CD1d knockout mice were resistant to UV-induced immunosuppression, prompting us to further address the role of CD1d in regulating UV carcinogenesis. We, therefore, investigated the response of wild-type (WT) and CD1d-/- mice to UV carcinogenesis.

Platelet activating factor receptor binding plays a critical role in jet fuel-induced immune suppression.

Applying military jet fuel (JP-8) or commercial jet fuel (Jet-A) to the skin of mice suppresses the immune response in a dose-dependent manner. The release of biological response modifiers, particularly prostaglandin E2 (PGE2), is a critical step in activating immune suppression. Previous studies have shown that injecting selective cyclooxygenase-2 inhibitors into jet fuel-treated mice blocks immune suppression.

In vivo expression of interleukin-8, and regulated on activation, normal, T-cell expressed, and secreted, by human germinal centre B lymphocytes.

T-cell homing within germinal centres (GCs) is required for humoral B-cell responses. However, the mechanisms implicated in the recruitment of T cells into the GC are not completely understood. Here we show, by immunohistology, and Northern and Western blots, that in vivo human GC B lymphocytes can express CxC and CC chemokines.

Determining the role of cytokines in UV-induced immunomodulation.

Ultraviolet radiation exposure damages DNA and promotes the development of skin cancer. In addition, UV exposure suppresses the immune response. Although the mechanism by which epidermal exposure to UV induces systemic immune suppression is not fully understood, it is clear that cytokines are involved.

Ultraviolet radiation-induced immunosuppression of delayed-type hypersensitivity in mice.

Ultraviolet (UV) radiation present in sunlight plays a critical role in the initiation and promotion of nonmelanoma skin carcinogenesis and immune suppression. The immune suppressive effects of UV have been identified as a risk factor for skin cancer induction. For these reasons, scientists have focused on elucidating the mechanisms of UV-induced immune suppression to better understand the pathogenesis of skin cancer induction.

Mechanisms underlying the suppression of established immune responses by ultraviolet radiation.

The ultraviolet radiation present in sunlight is immune suppressive. Recently we showed that solar-simulated ultraviolet radiation (ultraviolet A + B; 295-400 nm), applied after immunization, suppressed immunologic memory and the elicitation of delayed-type hypersensitivity to the common opportunistic pathogen, Candida albicans. Further, we found that wavelengths in the ultraviolet A region of the solar spectrum (320-400 nm), devoid of ultraviolet B, were equally effective in activating immune suppression as ultraviolet A + B radiation.

Dermal application of jet fuel suppresses secondary immune reactions.

Applying military jet fuel (JP-8) to the skin of mice activates systemic immune suppression. In all of our previous experiments, JP-8 was applied to immunologically naïve mice. The effect of jet fuels on established immune reactions, such as immunological memory, is unknown.

Platelet-activating factor, a molecular sensor for cellular damage, activates systemic immune suppression.

Ultraviolet (UV) radiation plays a critical role in the induction of nonmelanoma skin cancer. UV radiation is also immune suppressive, and the immune suppression induced by UV irradiation has been identified as a major risk factor for skin cancer induction. Previously, we showed that UV exposure activates a cytokine cascade involving prostaglandin (PG)E(2), interleukin (IL)-4, and IL-10 that induces immune suppression.