& Immunology Fun

So, tomorrow we have our papers for immunology class due; basically the papers are a summary of some line of research, which is semi-extra credit. We were paired off so that another student could give their feedback on our first drafts before turning in the final version. I found a pretty cool piece of research, and it seems I wasn't the only one. The abstract of the paper I found:

Lupus, a multigenic autoimmune condition in which a breakdown of tolerance results in the development of autoantibodies, leads to a variety of pathologic outcomes. Despite the heterogeneity of factors influencing disease susceptibility, we demonstrate that the partial restoration of inhibitory Fc receptor (FcgRIIB) levels on B cells in lupus-prone mouse strains is sufficient to restore tolerance and prevent autoimmunity. FcgRIIB regulates a common B cell checkpoint in genetically diverse lupus-prone mouse strains, and modest changes in its expression can result in either tolerance or autoimmunity. Therefore, increasing Fc{gamma}RIIB levels on B cells may be an effective way to treat autoimmune diseases.

What that means is that they managed to cure a class of autoimmune diseases by simply increasing expression of one receptor on B cells (antibody producing cells, basically). How cool is that?

The abstract of the article the person I'm paired with found:

Non-obese diabetic (NOD) mice develop spontaneous T-cell responses against pancreatic beta cells, leading to islet cell destruction and diabetes. Despite high genetic similarity, non-obese resistant (NOR) mice do not develop diabetes. We show here that spleen cells of both NOD and NOR mice respond to the islet cell antigen glutamic acid decarboxylase-65 in IFN-gamma-ELISPOT assays. Moreover, NOR-T cells induce periinsulitis in NOD SCID recipient mice. Thus, a potentially pathogenic islet cell-specific T-cell response arises in NOR and NOD mice alike; the mechanism that prevents the autoimmune progression of self-reactive T cells in NOR mice presumably acts at the level of effector function. Consistent with this hypothesis, CD4+CD25+ cell-depleted spleen cells from NOR mice mediated islet cell destruction and overt diabetes in NOD SCID mice. Therefore, islet cell-specific effector cells in NOR mice appear to be under the control of CD4+CD25+ regulatory T cells, confirming the importance of regulatory cells in the control of autoimmune diabetes.

What that means: there are two strains of mice, one (NOD) which is prone to diabetes, the other (NOR) not, yet the two strains are extremely similar to each other genetically. In both strains the immune system builds up in preparation to attack insulin-producing cells in the pancreas (the cause of this type of diabetes), but in only one of the strains (NOD) does it actually attack. The exact reason for this is unknown, but it seems to have something to do with one type of immune cell (CD4+, CD25+ T cells).

I thought this one line from the article was humorous: "...would permit to address this hypothesis." Can't find a pronoun that fits? Just omit it completely!

Lastly, note that these papers can be thought of as press-releases. The authors may claim things that are/could be wrong. For example, in the first article they used four different strains of mice in the experiment, which consisted of collecting data a good dozen ways. However, not all of the data is shown for all four strains; some data they only show data for one strain. I wonder why.