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Innate Immunity: The Bridge between Adaptive Immunity and Inflammation, December 17, 1998, New York Academy of Sciences, New York, NY, USA
| Content Provider | Semantic Scholar |
|---|---|
| Author | Barton, Beverly E. |
| Copyright Year | 1999 |
| Abstract | ing about innate immunity, adaptive immunity, and inflammation on December 17, 1998 at the New York Academy of Sciences (New York, New York, USA). Presentations showed how the innate immune response leads to inflammation at the same time it allows the development of the anamnestic immune response. Dr. Patricia Fitzgerald-Bocarsly, Department of Pathology and Laboratory Medicine, New Jersey Medical School (Newark, NJ, USA), presented first. Her work focused on the innate response to viruses. A prominent cell type involved in the immediate response to viral pathogens is the NK (“null killer”) cell, so-called because it lacks the surface phenotypic markers found on most lymphocytes. It has been shown that although purified NK cells can lyse tumor cell targets in vitro, the same population of cells doesn’t lyse virally-infected targets. Addition of an HLA-DR+ accessory cell from the blood to NK cells allows lysis of virally-infected targets by NK cells. The accessory cells were found to be a “lymphoid”type dendritic cells which circulates in the blood; it is not the same cell type as the antigen-presenting dendritic cells in lymph nodes [1]. The lymphoid dendritic cell is the source of interferon-a, which is required to activate the NK cell so it can lyse virally-infected targets; interferon-a is not required for NK cell lysis of tumor targets because different pathways for killing target cells are used by NK cells, depending upon whether the target is a neoplastic cell or one infected by viruses [2]. The pathways are distinguished by the sensitivity of NK cell-mediated viral target lysis by wortmannin, an inhibitor of the phosphoinositol-3-kinase signalling cascade. When wortmanin is added to co-cultures of NK cells, accessory cells, and viral targets, lysis of the target cells does not occur, yet addition of wortmannin to co-cultures of NK cells and tumor cells does not affect the killing of the tumor cells by the NK cells. Having two pathways leading to cell lysis, one of which requires an accessory cell, is probably a regulatory mechanism to prevent uncontrolled lysis of by-stander cells, which could lead to destruction of tissue [3]. Besides interferon-a, the accessory cell produces other factors which lead to NK cell activation for lysis of viral targets. Among these are interleukin (IL-) 12 and IL-2. The addition of any one of these 3 cytokines to co-cultures of NK cells plus virally-infected target cells causes the lysis of the target cells by NK cells. Wortmannin does not affect synthesis and release of interferon-a by accessory cells, rather it inhibits the activation of NK cells by released cytokine. Interferon-a is the protein produced in highest amounts by activated accessory cells. They have been found, by an ELISA technique, to make 3 to 5 pg of interferon-a per cell which allows one to score the production of factors by single cells. Lymphoid dendritic cells occur at very low frequency in the blood. They have been found at a frequency of just 0.1% of the peripheral blood leukocytes [1]. Their rarity has made definitive research on their receptors, signalling pathways, etc. extremely difficult to perform. Although these accessory cells have been named “lymphoid” they are almost certainly of the myeloid, not lymphoid, lineage. Recently, work has begun to enumerate and study the function of lymphoid dendritic cells in HIV+ patients, in order to determine if boosting NK cell function can eliminate virus before the progression to AIDS has occurred [4]. Dr. Gill Diamond, Department of Anatomy, Cell Biology, and Injury Sciences, New Jersey Medical School (Newark, NJ, USA), presented recent work on anti-microbial peptides, defensins, found in the trachea of cattle, and which have human homologues as well. Defensins are small proteins, with highly-conserved sequences, which are expressed in many vertebrates. Mostly they are produced by neutrophils. Recently it was discovered that tracheal epithelium produces its own type of defensin. This was accomplished by fractionating homogenates of bovine trachea and screening for Inflamm. res. 48 (1999) 232–235 1023-3830/99/050232-04 $ 1.50+0.20/0 © Birkhäuser Verlag, Basel, 1999 |
| Starting Page | 232 |
| Ending Page | 235 |
| Page Count | 4 |
| File Format | PDF HTM / HTML |
| DOI | 10.1007/s000110050451 |
| PubMed reference number | 10391109 |
| Journal | Medline |
| Volume Number | 48 |
| Alternate Webpage(s) | https://page-one.springer.com/pdf/preview/10.1007/s000110050451 |
| Alternate Webpage(s) | https://doi.org/10.1007/s000110050451 |
| Journal | Inflammation Research |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
