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It is well-recognized that human immunodeficiency virus type-1 (HIV-1) mainly targets CD4 T cells and macrophages. Nonetheless, during the past three decades, a huge number of studies have reported that HIV-1 can directly or indirectly target other cellular components of the immune system including CD8 T cells, B cells, dendritic cells, natural killer cells, and polymorphonuclear neutrophils (PMNs), among others. PMNs are the most abundant leukocytes in the human circulation, and are known to play principal roles in the elimination of invading pathogens, regulating different immune responses, healing of injured tissues, and maintaining mucosal homeostasis. Until recently, little was known about the impact of HIV-1 infection on PMNs as well as the impact of PMNs on HIV-1 disease progression. This is because early studies focused on neutropenia and recurrent microbial infections, particularly, during advanced disease. However, recent studies have extended the investigation area to cover new aspects of the interactions between HIV-1 and PMNs. This review aims to summarize these advances and address the impact of HIV-1 infection on PMNs as well as the impact of PMNs on HIV-1 disease progression to better understand the pathophysiology of HIV-1 infection.

Chronic immune activation and inflammation are unwanted consequences of many pathological conditions, since they could lead to tissue damage and immune exhaustion, both of which can worsen the pathological condition status. In fact, the immune system is naturally equipped with immunoregulatory cells that can limit immune activation and inflammation. However, chronic activation of downregulatory immune responses is also associated with unwanted consequences that, in turn, could lead to disease progression as seen in the case of cancer and chronic infections. Myeloid-derived suppressor cells (MDSCs) are now considered to play a pivotal role in the pathogenesis of different inflammatory pathological conditions, including different types of cancer and chronic infections. As a potent immunosuppressor cell population, MDSCs can inhibit specific and non-specific immune responses via different mechanisms that, in turn, lead to disease persistence. One such mechanism by which MDSCs can activate their immunosuppressive effects is accomplished by secreting copious amounts of immunosuppressant molecules such as interleukin-10 (IL-10). In this article, we will focus on the pathological role of MDSC expansion in chronic inflammatory conditions including cancer, sepsis/infection, autoimmunity, asthma and ageing, as well as some of the mechanisms by which MDSCs/IL-10 contribute to the disease progression in such conditions.

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The results of this study emphasized the importance of contact infections, namely contact with infected animals and their products, as a method of transmission of brucellosis compared to ingestion of contaminated animal products.

In perchloric acid extracts of normal lung and colonic tumors, 3 NCA molecules were identified by monoclonal antibodies that cross-reacted with CEA, which itself gave 2 bands in SDS-PAGE. The proteins had molecular weights of 50, 75 and 97 kd, while the 2 CEA molecules banded at 180 and 160 kd in SDS-PAGE. No MAb recognized only one molecule, with the exception of MAb 3/13 which precipitated solely the upper CEA band. Analysis of the biochemical relationship of the cross-reactive antigens showed that none of them contained any internal methionine. Furthermore, after digestion by thermolysin, the peptide maps of the immunoprecipitated molecules showed very close similarities, if not identity. When the cross-reactive and the CEA were compared, the only differences found were in the upper CEA band, which apparently lacked one hydrophobic peptide, while the 97 kd cross-reacting protein showed one extra peptide. We conclude from our results that CEA and the cross-reacting molecules are composed of nearly identical, small (i.e. less than 50 kd) polypeptide chains.

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