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Showing posts with label pregnancy. Show all posts
Showing posts with label pregnancy. Show all posts

Tuesday, November 12, 2013

Maternal Regulatory T Cells: One of Mother’s (and Baby’s) First Lines of Defense

Maternal regulatory T cells play a vital role in maintaining maternal-fetal tolerance and sustaining pregnancies.  By better understanding the mechanisms by which maternal regulatory T cells mediate immune reactions during pregnancy and how pathogens manipulate such immune reactions, it is possible to develop preventative measures against opportunistic pathogens that target mothers during this critical period of time.
In many ways, the immune system’s response to pregnancy is akin to that of organ transplantation; the maternal immune system must determine if the growing fetus poses a threat to the mother’s own survival and if it must be rejected (Gobert and Lafaille 2012). This problem results from the fetus being semiallogenic in nature, meaning that it expresses a combination of both maternal and paternal antigens (Gobert and Lafaille 2012). However, despite the fact that the paternal antigens are considered foreign by the maternal immune system, most maternal immune systems do not cause significant damage to the developing fetus.  This is made possible by the establishment of maternal-fetal tolerance, which increases the probability that the mother’s body will instead perceive the baby as “temporary self” (Trowsdale and Betz 2006).  However, establishing a maternal-fetal tolerance puts the mother at risk by limiting the capacity of her immune system to identify other foreign pathogens that could cause her harm.  Therefore, many non-overlapping mechanisms have evolved to maintain a delicate balance between immunosuppression – to protect the fetus from the maternal immune systems – and immune reactivity – to protect both mother and child from invading pathogens (Munoz-Suano, Hamilton and Betz 2011).   Recent research into maternal-fetal tolerance seeks to shed some light on these mechanisms, particularly those mediated by a subpopulation of T cells called regulatory T cells (Tregs) (Gobert and Lafaille 2012, Munoz-Suano, Hamilton and Betz 2011, Rowe, et al. 2013).

Wednesday, December 14, 2011

The Joy of Pregnancy: Relief of Rheumatoid arthritis symptoms during pregnancy

AIDS, multiple sclerosis, type 1 diabetes, Rheumatoid Arthritis (RA). You might be wondering where this seemingly depressing list is heading, and that’s a fairly reasonable question. Each of these diseases is an autoimmune disease, meaning that the ones immune system is attacking its own body as if it were foreign. You might be familiar with some more than others, perhaps through the media, or through family and friends. What you might not know, is what kind of therapeutic agents are being employed in combating these diseases. One disease in particular, Rheumatoid Arthritis, affects ones joints, and causes a very painful inflammation as your body attacks its own joint tissues.1 While this doesn’t typically onset until later in one’s life, women in childbearing age can be affected. One phenomenon which has been observed is an actual regression of RA symptoms and potentially remission2. Unfortunately, the symptoms are reported to return post pregnancy.3 This then leads to the question what is happening during pregnancy that alleviates the symptoms and in some cases causes remission.
Many studies have been conducted to answer such a question, and the results are highly variable. Some studies point out that a certain type of immune cells, Th1, and its reduction during pregnancy may be responsible for the alleviation and remission of rheumatoid arthritis and symptoms.4 One particular study seeks to investigate the effects of regulatory T cells (Tregs) and how they might be interrupting the deleterious effects exhibited in RA. Whatever it may be that these studies are attempting to credit with the beneficial effects of pregnancy, they all work towards understanding the disease in order to understand how to better prevent it. If the immune system of pregnant women is able to “fight” off RA, perhaps understanding the mechanism will allow insight into how this can be converted into a publicly available treatment.

Saturday, November 26, 2011

Protect Your Unborn or Newborn Baby: Secondhand Smoking’s Association to Asthma


Do you know someone with asthma? Chances are that you do. In 2009, over 8% of the US population reported that they currently had asthma. Interestingly, asthma rates are the highest among children and teenagers (Akinbami et al., 2011). Allergic asthma in particular is the type of asthma that is most commonly found in children. Allergic asthma, also known as atopic asthma, affects the lower respiratory tracts. Inhalation of an allergen leads to the release of granules from sensitized cells called mast cells that are located in the mucus of a person’s nose or bronchi (which serve as passageways into his or her lungs). The release of these granules and other molecules favour inflammation. This causes abundant amounts of mucus to be secreted and the tightening of a person’s airways. Asthmatics routinely report feelings of constriction in their chest as well as wheezing. Given this information, you might ask the following question: what factors contribute to the development of allergic asthma? Exposure to cigarette smoke during fetal development and during a child’s infancy has been shown to be a risk factor for allergic asthma (DiFranza et al., 2004). Mice exposed to secondhand smoke (SS) early-on after birth also seem to develop respiratory infections (Phaybouth et al., 1006), and can be used as a model for this disease. The specific contributions of exposure to smoke that is either prenatal (before birth) or early postnatal (after birth) in the development of allergic asthma, however, is not well understood. Also, the specific way in which exposure to cigarette smoke leads to asthma is not understood in great detail. To shed some light on these topics, researchers decided to use a mouse model to study the development of allergic asthma (Singh et al. 2011).