Generalized eczematous rash in a patient with shoe contact dermatitis: a case report

The id reaction, which is also known as autoeczematisation or autosensitisation dermatitis, refers to the acute development of dermatitis at a site distant from the site of the primary inflammatory cutaneous reaction. Many stimuli have been reported as causes of id reactions, including allergic contact dermatitis. The exact prevalence of id reaction is unknown, however, id reactions have been found to occur in 4%-5% of cases of dermatophyte infections and in up to 37% of patients with stasis dermatitis. This condition has no known predilection for any race, sex or age groups. Shoe dermatitis is a type of contact dermatitis developed following the contact of the foot’s skin with shoe’s parts that contain different chemical substance that harbor the potentiality to be an immune trigger. Among the potential allergens, rubber is found to be the most common shoe-related allergen reported in the literature. Other known allergens include: cements, dichromats used in tanning, dyes, anti-mildew agents, formaldehyde, and nickel eyelets or nickel arch supports. The pathogenesis of allergic contact dermatitis is a type IV, delayed-type immune response that provoked by cutaneous contacts with different material that have the ability to stimulate antigen-specific T-helper 1 (TH1) in a sensitized individual. The clinical presentation of id reaction includes acute onset of pruritic erythematous eruption with symmetrical distribution that follows the primary dermatitis by one to two weeks. Authors report a 27-year-old male who presented with generalized, symmetric pruritic and eczematous eruption following localized shoe dermatitis.

Is infant immunization by breastfeeding possible?

Breastfeeding is known as the most efficient way to prevent infectious disease in early life. Maternal anti-microbial immunoglobulins transfer through milk confers passive immunity to the breastfed child while his immune system is maturing. Maternal milk also contains bioactive factors that will stimulate this maturation. From the literature on breastfeeding prevention of immune-mediated disease and more specifically from our experiments conducted in the field of allergic disease prevention, we propose that breastfeeding may also induce antigen-specific immune responses in the breastfed child. We found that early oral antigen exposure through breast milk leads to tolerance or immune priming depending on the nature of the antigen transferred and accompanying maternal milk cofactors. Here, we will discuss our data in the light of prevention of infectious disease and will propose that possible milk transfer of microbial antigen could affect actively the immune response in breastfed children and thereby their long-term susceptibility to infectious disease. Further research in this direction may lead to novel strategies of early life vaccination, taking advantage of the possibility to stimulate antigen-specific immune responses through breast milk.

Pilot study of MAGE-A3 protein vaccination and autologous stem cell transplantation (autoSCT) as consolidation therapy for multiple myeloma (MM).

TPS8111 Background: MAGE-A3 is a cancer-testis antigen (CT Ag) commonly expressed in MM but not in normal non-gonadal tissues. MAGE-A3 inhibited p53-dependent and independent apoptosis in MM cells (Clin Cancer Res 2011;17:4309), and spontaneous immunity against CT Ags in MM patients was associated with favorable clinical outcomes (Blood 2007;109:1103; Blood 2008;112:3362), making it a rational target for immunotherapy. In this study (NCT01380145), we are examining if a recombinant (rec) MAGE-A3 protein vaccine + adjuvant combined with vaccine-primed peripheral blood lymphocytes (PBL) can safely stimulate antigen-specific immunity in MM patients undergoing autoSCT for consolidation therapy. Methods: Patients meeting the following criteria are eligible: within 12 months of diagnosis; MAGE-A+ MM cells by immunohistochemistry; achieving at least a very good partial response with induction therapy; and meeting institutional criteria for autoSCT. One patient of a planned cohort of sixteen has been enrolled. Six weeks before SCT, subjects will receive their first vaccination (300 μg IM) and three weeks later undergo leukopheresis to collect vaccine-primed PBL. They then undergo stem cell mobilization followed by a standard melphalan-conditioned autoSCT. On day 3 after stem cell infusion, the unmanipulated, primed PBL will be re-infused followed by the second recMAGE-A3 vaccination on day 10. An additional six vaccinations will be administered on days 31, 52, 73, 94, 180, and 270 after autoSCT. The primary objectives are safety and tolerability. The secondary objectives of cellular and humoral immune responses and lymphocyte reconstitution will be assessed by a validated series of quantitative assays using established response criteria (PNAS 2008;105:1650). Success criteria based on immune response have not been specified for this pilot study, though induction of MAGE-A3 immunity in at least 50% of patients would merit consideration for further evaluation of clinical efficacy.

Platelet-mediated modulation of adaptive immunity: unique delivery of CD154 signal by platelet-derived membrane vesicles

Although mounting evidence indicates that platelets participate in the modulation of both innate and adaptive immunity, the mechanisms by which platelets exert these effects have not been clearly defined. The study reported herein uses a previously documented adoptive transfer model to investigate the ability of platelet-derived membrane vesicles to communicate activation signals to the B-cell compartment. The findings demonstrate for the first time that platelet-derived membrane vesicles are sufficient to deliver CD154 to stimulate antigen-specific IgG production and modulate germinal center formation through cooperation with responses elicited by CD4+ T cells. The data are consistent with the hypothesis that platelets modulate inflammation and adaptive immunity at sites distant from the location of activation and that platelet-derived membrane vesicles are sufficient to mediate the effect.