It seems to me that almost everybody nowadays has either a food allergy, seasonal allergy, or both. Therefore, it becomes more important to understand the mechanism of allergies so that we can better treat them. This paper examined the effect of the natural killer (NK) cell receptor NKD2G on pulmonary inflammation caused by allergic reactions.
Allergies are a type of type 1 immune hypersensitivity (HS1). There are two stages of HS1: sensitization and effector. During the sensitization stage, the allergen is gathered by dendritic cells which move to the lymph node where they present the allergen to naïve Th cells. These Th cells then provide T-cell help to B cells which release homing cytokines for other leukocytes to follow. Other immune cells produce IL-4, IL-5 and IL-13 which facilitate isotype switching to IgE antibodies. These antibodies then bind to receptors on the surface of basophils and mast cells. The effector stage is the second exposure to the allergen. The IgE antibodies bound to mast cells recognize the allergen and cause degranulation of the mast cells which have different effects depending on the tissue in which this is occurring.1
This video might help you understand immune hypersensitivity better as well:
The first experiment performed examined how NKG2D regulated the pulmonary inflammation caused by house dust mites (HDM). HDM extract was given to mice that lacked the NKG2D receptor (klrkl-/-) and compared to those that had the receptor (klrkl+/+). As a result, klrkl-/- mice showed a greatly reduced inflammatory response when compared to klrkl+/+ mice. Additionally, there was less protein exudate in the airway when measured in the bronchoalveolar lavage (BAL) and significantly diminished recruitment of neutrophils, eosinophils and lymphocytes in klrkl-/- mice. Furthermore, of the CD4+ T cells that were recruited in klrkl-/- mice, much less IL-4 and IL-13 was secreted proportionally when compared to klrkl+/+mice.2
However, eliminating one gene completely, as in the NKG2D deficient mice, could have confounding effects that could be the cause of results above. In fact, the results above could indicate that the absence of NKD2G caused a decrease in NK cells immune response and not because it was involved in pulmonary inflammation. To rule out this possibility, both klrkl+/+ and klrkl-/- mice were infected with respiratory syncytial virus and the viral load and immune response was measured after four days. The results showed that there was not a difference between the two groups of mice in either viral load or in CD4+ and CD8+ T cell development. The results obtained demonstrate that mice can still have an immune response in the absence of NKD2G. This means that the results obtained when NKD2G lacking mice were injected with HDM extract are from the role of NKD2G in allergic inflammation.2
Additionally, using flow cytometry with a gate for NKD2G expression, it was determined which cells expressed NKD2G. This revealed that 80% of cells expressing NKD2G are NK cells with small amounts present on CD4+ and CD8+ T-cells, Also, the transfer of wild-type NK cells into klrkl-/- mice caused allergic pulmonary inflammation to be restored, thus further indicating the role of NKD2G in allergic inflammation.2
Knowing that in the NKD2G is involved in causing allergic inflammation, it could become a target to help temporarily treat allergies. If its function can be inhibited, then the impact that allergies have on people’s lives could be reduced.
Mak, Tak W., and Mary E. Saunders. Primer to the Immune Response: Academic Cell Update. Burlington: Elsevier, 2011. Print.
Farhadi, Nazanin, Laura Lambert, Chiara Triulzi, Peter J.M. Openshaw, Nadia Guerra, and Fiona J. Culley. "Natural Killer Cell NKG2D and Granzyme B Are Critical for Allergic Pulmonary Inflammation." Journal of Allergy and Clinical Immunology (2013): n. pag. ScienceDirect. Elsevier B.V., 28 Nov. 2013. Web. 10 Dec. 2013. <http://www.sciencedirect.com/science/article/pii/S0091674913015558>.