Palestinian Refugee Camps: from Shelter to Habitat

Palestinian refugees registered with UNRWA and their housing conditions are officially characterized by a “ temporary status” , a situation which has lasted the past sixty years. This article explores this time-paradox by focusing on the host governments’ and UNRWA’s policies affecting the refugees’ housing conditions. After having reviewed available literature, this contribution analyses the current housing situation. Drawing on data from a recent survey, the authors provide insights on areas where intervention is needed. In all UNRWA’s fields of operation, overcrowding, lack of public spaces, humidity and structural defects are the main sources of housing discomfort that camp refugees endure. Host countries’ restrictions as well as the incapacity or unwillingness of larger urban municipalities to incorporate refugee camps in their master plans are among the main obstacles to the refugees’ housing development. Rehabilitation and self-help re-housing programs may offer substantial incentives for housing improvement. The success of such programs depends, among several factors, on the host governments’ good will to provide UNRWA with authorizations, financial support, and land, as well as on the capacity of involving the refugee communities in projects’ planning and implementation.

Destruction of lymphoid organ architecture and hepatitis caused by CD4+ T cells

Immune responses have the important function of host defense and protection against pathogens. However, the immune response also causes inflammation and host tissue injury, termed immunopathology. For example, hepatitis B and C virus infection in humans cause immunopathological sequel with destruction of liver cells by the host's own immune response. Similarly, after infection with lymphocytic choriomeningitis virus (LCMV) in mice, the adaptive immune response causes liver cell damage, choriomeningitis and destruction of lymphoid organ architecture. The immunopathological sequel during LCMV infection has been attributed to cytotoxic CD8(+) T cells. However, we now show that during LCMV infection CD4(+) T cells selectively induced the destruction of splenic marginal zone and caused liver cell damage with elevated serum alanin-transferase (ALT) levels. The destruction of the splenic marginal zone by CD4(+) T cells included the reduction of marginal zone B cells, marginal zone macrophages and marginal zone metallophilic macrophages. Functionally, this resulted in an impaired production of neutralizing antibodies against LCMV. Furthermore, CD4(+) T cells reduced B cells with an IgM(high)IgD(low) phenotype (transitional stage 1 and 2, marginal zone B cells), whereas other B cell subtypes such as follicular type 1 and 2 and germinal center/memory B cells were not affected. Adoptive transfer of CD4(+) T cells lacking different important effector cytokines and cytolytic pathways such as IFNγ, TNFα, perforin and Fas-FasL interaction did reveal that these cytolytic pathways are redundant in the induction of immunopathological sequel in spleen. In conclusion, our results define an important role of CD4(+) T cells in the induction of immunopathology in liver and spleen. This includes the CD4(+) T cell mediated destruction of the splenic marginal zone with consecutively impaired protective neutralizing antibody responses.

Tributary and Mainstem Benthic Macroinvertebrate Communities Linked By Direct Dispersal and Indirect Habitat Alteration

Benthic communities in tributary-mainstem networks might interact via downstream drift of invertebrates or material from tributaries and adult dispersal from the mainstem. Depending on the strength of these interactions, mainstem downstream communities are expected to be more similar to tributary communities due to drift or habitat alteration. Communities not connected by flow are expected to be similar due to adult dispersal but decreasing in similarity with distance from the mainstem. We investigated interactions between invertebrate communities of a 7th order river and 5th order tributary by comparing benthic community structure in the river upstream and downstream of the tributary confluence and upstream in the tributary. Non-metric multidimensional scaling showed invertebrate communities and habitat traits from river locations directly downstream of the tributary clustered tightly, intermediate between tributary and mid-channel river locations. In addition, Bray-Curtis dissimilarity increased between the mainstem and tributary with distance upstream in the tributary. Our results indicate that similarities between mainstem and tributary communities are potentially caused by direct mass effects from tributary to downstream mainstem communities by invertebrate drift and indirect mass effects by habitat restructuring via material delivery from the tributary, as well as potential effects of adult dispersal from the river on proximal tributary communities.

The habitat, double life, citizenship, and forgetfulness of IgA

Immunoglobulin A (IgA) is the main secretory immunoglobulin of mucous membranes and is powerfully induced by the presence of commensal microbes in the intestine. B cells undergo class switch recombination to IgA in the mucosa-associated lymphoid tissues, particularly mesenteric lymph nodes (MLNs) and Peyer's patches, through both T-dependent and T-independent pathways. IgA B cells primed in the mucosa traffic from the intestinal lymphoid structures, initially through the lymphatics and then join the bloodstream, to home back to the intestinal mucosa as IgA-secreting plasma cells. Once induced, anti-bacterial IgA can be extremely long-lived but is replaced if there is induction of additional IgA specificities by other microbes. The mucosal immune system is anatomically separated from the systemic immune system by the MLNs, which act as a firewall to prevent penetration of live intestinal bacteria to systemic sites. Dendritic cells sample intestinal bacteria and induce B cells to switch to IgA. In contrast, intestinal macrophages are adept at killing extracellular bacteria and are able to clear bacteria that have crossed the mucus and epithelial barriers. There is both a continuum between innate and adaptive immune mechanisms and compartmentalization of the mucosal immune system from systemic immunity that function to preserve host microbial mutualism.