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Non-bilayer phospholipids arrangements (NPAs) are transient molecular associations different from lipid bilayers. When they become stable, they can trigger a disease in mice resembling human lupus, which is mainly characterized by the production of anti-NPA IgG antibodies. NPAs are stabilized on liposomes or cell bilayers by the drugs procainamide or chlorpromazine, which produce drug-induced lupus in humans. Here, we evaluated the participation of the TH 2 response, through its hallmark cytokine IL-4, on the development of the lupus-like disease in mice. Wild-type or IL-4 knockout BALB/c mice received liposomes bearing drug-induced NPAs, the drugs alone, or an anti-NPA monoclonal antibody (H308) to induce the lupus-like disease (the last two procedures stabilize NPAs on mice cells). IL-4 KO mice showed minor disease manifestations, compared to wild-type mice, with decreased production of anti-NPA IgG antibodies, no anti-cardiolipin, anti-histones and anticoagulant antibodies, and no kidney or skin lesions. In these mice, H308 was the only inducer of anti-NPA IgG antibodies. These findings indicate that IL-4 has a central role in the development of the murine lupus-like disease induced by NPA stabilization.

In Europe, the stem and bulb nematode Ditylenchus dipsaci has been listed as a quarantine pest by EPPO: without any control, it may cause complete failure of alfalfa crops. Movement of nematodes associated with seeds is considered to be the highest-risk pathway for the spread of this pest. Since the 2010 official withdrawal of methyl bromide in Europe, and in the absence of any alternative chemical, fumigation of contaminated seed batches is no longer possible, which makes the production of nematode-free alfalfa seeds difficult to achieve and leads to unmarketable seed batches. Thermotherapy is being considered as a realistic alternative strategy, but its efficiency still remains to be validated. The combination of the currently available methods (i.e. use of resistant cultivars, seed production according to a certification scheme, mechanical sieving, seed batch inspection) could significantly reduce the likelihood of seed contamination. However, it does not guarantee a total eradication of the nematode. Although it is already widely distributed all over Europe, reclassification of D. dipsaci as a regulated non-quarantine pest to reduce the possibility of further introductions and the rate of spread of this pest appears to be a risky strategy because of the lack of up-to-date documented data to evaluate damage thresholds and determine acceptable tolerance levels.

The aim of the present study was to reevaluate the distribution of HLA antigens in Mexican Mestizos since, in our previous report, very few specificities were explored for this population. The Mestizos are primarly a mixture of Caucasians (Spaniards) and Mexican Indians and account at the present time for about 95% of the total Mexican population. A and B antigens were typed on isolated cells using a microlymphocytotoxicity technique. Antigen, gene and haplotype frequencies were calculated including the significance for delta values. The results clearly showed that the HLA distribution differs from other ethnic groups and the predominant antigens are A2, A9, B5, Bw35 and B40, but the general pattern clearly shows the participation in genetical composition of Spanish and Mexican Indian backgrounds. The most frequent haplotypes were A2-B5, A9-Bw35, A9-B40 and A2-B40, which are also the most common in some Mongoloid populations.

In humans, T cells expressing the CD161 molecule NKR-P1A constitute around 20% of the circulating CD3(+) cells and are potentially immunoregulatory in several diseases. Their role in asthma is not well known, but they could participate in asthma attacks. To determinate whether activation of CD161(+) T cells and their cytokine production correlate with clinical status of asthma, we analysed blood samples from asthma attack patients (AAP) and stable asthma patients (SAP) in comparison with healthy non-atopic controls (HC). There was a significant higher baseline expression of CD69 on T cells from AAP and the difference was more notorious on CD161(+) T cells; upregulation of CD69 was observed on both CD161(-) and CD161(+) T cells driven by Dermatophagoides pteronyssinus crude extract, whereas polyclonal stimulation with phorbol 12-myristate 13-acetate plus ionomycin predominantly induced IFN-gamma but no IL-4, IL-5 and IL-13 by CD161(+) T cells in all groups; upon polyclonal stimulation, there were more CD161(+) T cells producing IFN-gamma and less CD161(-) T cells producing this cytokine, contrasting with the opposite results observed in SAP and HC groups. Our results indicate that, during asthma attack, CD161(+) T cells are activated and are able to produce predominantly IFN-gamma but no Th2 cytokines. We hypothesize that during an asthma attack, IFN-gamma produced by CD161(+) T cells could help to reestablish the Th1/Th2 equilibrium. These observations may contribute to the understanding of the immune mechanisms involved in asthma attacks.

Dengue virus (DV) infections are serious causes of morbidity and mortality worldwide, and adaptive (secondary) immune response appears to influence the severity of this arboviral disease (Morens 1994; Halstead & O'Rourke 1977; Rigau-Perez et al. 1998). There are an estimated 50–100 million cases of dengue fever and 250,000-500,000 cases of dengue haemorrhagic fever (DHF) annually in the world (WHO 1997). The dengue shock syndrome (DSS), the most severe and potentially fatal form of the disease, especially in developing countries, is less frequent. In the model proposed here, we have chosen to examine DV2, because it is the prevalent serotype (Gomez-Dantes et al. 2004). The high seroprevalence together with the co-circulation of multiple serotypes indicates that Mexico could be in risk of an important DHF outbreak (Gomez-Dantes et al. 2004). The exact pathogenic mechanisms following DV infection are not well understood, especially in the severe forms of the infection (DHF and DSS). The immune response to DV seems at least partially involved in the process (Halstead 1988; Avirutnan et al. 1998; Diamond et al. 2000). Several theories have been advanced including facilitation of DV infection by non-neutralizing antibodies (Halstead & O'Rourke 1977; Halstead et al. 1977; Morens 1994), the potential differential virulence of each infecting serotype (Leitmeyer et al. 1999; Kawaguchi et al. 2003), CD4-CD8 T-cell cross-reactivity and host factors such as a particular, but yet undefined susceptibility (Klenerman & Zinkernagel 1998; Mongkolsapaya et al. 2003). While there is an excellent research on dengue about the molecular structure and epidemiology of this virus, the basic mechanisms of the immunopathology still remain obscure (Haywood 1994; Kuhn et al. 2002). For instance, until very recently (Johnston et al. 2000; Wu et al. 2000), it was unknown whether DV was able to replicate in cutaneous cells. Likewise, there are two other features largely unexplored regarding DV infection: (i) the very early stages of the infection, because, by necessity, patients are examined when disease is almost over, when the patients are under recovery or when they have entered into DSS and (ii) which type of responses, if any, occur cutaneously, in situ, following DV inoculation when mosquitoes feed. We wanted to develop an in situ approach that would enable us to study the early immune pathology of the cellular events regarding the infectious process and the first reactions of the peripheral immune system, the dendritic cells (DCs). DCs constitute a system of highly dynamic sentinel cells, whose most studied element in peripheral non-lymphoid tissues is the epidermal Langerhans cells (LCs). It is now known that LCs perform multiple tasks including antigen capturing and processing, antigen ferrying to regional lymphoid tissues, and ultimately, cognate antigen presentation to naive lymphocytes, once in secondary lymphoid organs (Flores-Romo 2001). Under the influence of a variety of stimuli such as cytokines, antigens or microbial products, LCs become activated, start to migrate into the dermis and concomitantly to up-regulate antigen-presenting molecules and to express co-stimulatory and maturation markers (Cumberbatch & Kimber 1992; Cumberbatch et al. 1997). Nevertheless, despite that LCs as sensors of the external antigenic world are the most exposed cells of the immune system during mosquito feeding, and the initial virus inoculation through skin, the interactions of these cells with DV and the outcome of such potential interplay regarding both the virus and the LC have received little attention in situ (Wu et al. 2000). We attempted to address some of these issues by establishing a model with fresh, healthy, non-cadaveric human skin explants exposed to DV, to analyse whether local infection and viral replication are feasible experimentally, to assess the most early phases of the initiation of the immune responses in situ and the immediate local repercussions of viral inoculation upon local antigen-presenting cells (APCs), particularly on the DCs, the sentinel posts of the immune system in the skin.