Mice that live for a short duration of time develop fevers to counter-act the effect of antigens. Developing fevers is a sort of a brute force method to get rid of infection as fevers cause native tissue damage in the process. But for animals that are short-lived, the collateral damage is of lesser importance. Long-lived animals on the contrary, rely on developing antibodies to counter antigens.

The infiltration of CD11b+Gr+ myeloid cells in tumors causes the tumors to be non-responsive towards anti-angiogenic VEGF treatment. A combination therapy comprising of anti-VEGF and mab against myeloid cells causes the suppression of tumor growth more effectively than anti-VEGF alone.

Two complementary determining regions (CDRs) separated by a framework region (FR) retain the specificity of the parental antibody. The entire construct is just 28 amino acids long. Conjugating this shortened antibody to a toxin led to the regression of tumors in vivo.

During inflammatory disorders, the level of TNF-alpha goes up and higher levels of TNF-alpha causes fatigue and sleepiness.

When APCs process antigens in the endosomes, they activate effector T cells (CD8) and when they process in the lysosomes, the helper T cells (CD4) get activated

The paper reports a new insight into the link between atherosclerosis and inflammatory response. The authors developed a mouse model that had an excess of an immune cell called LIGHT (??). LIGHT cells are associated with liver function. When fed with a normal diet, the fat content was higher than wt mice on high fat. In interfering in the pathway by which LIGHT could activate the immune system, the fat content in the blood was lowered. The hypothesis put forward is that LIGHT cells prevent liver from metabolizing cholesterol and hence cholesterol ends up in the blood.

RBCs have antigens and based on the type of antigen, blood is classified into A, B, AB. If there are no antigens the type is O. Scientists have discovered enzymes that cleave off these antigens from the surface of the cells making them "immune tolerant".

When a T-cell comes in contact with an APC it forms an immunological synapse. The formation of this synapse is characterized by the asymmetrical distribution of protiens like CD4, CD8 adhesion molecules etc. Moreover, the cytoskeleton also rearranges itself during the synapse formation. The authors in this paper answered an important question. How does an activated T cell give rise to two distinct populations with different life spans? They found out that when the activated T cell (with an immunological synapse) divides, the daughter cell that was adjacent to the synapse forms the short-lived effector cells and the other cell forms the long-lived memory cells.

David Schneider at Stanford studied the possibility of vaccination in fruit flies. They first injected a non-lethal dose of S. pneumoniae in fruit fly and then subsequently injected a lethal dose. What they found was that the fruit flies did not get infected by the lethal dose and they lived as long as the control group. The vaccination was specific for S. pneumoniae and other pathogens killed the flies. Fruit fly, an invertebrate animal, does not have the adaptive immune system which is believed to be responsible for immunological memory in vertebrates. This suggests that the innate immune system (macrophages, complement, basophils. neutrophils and eosinophils) can form immunological memory. A significant find.

Calorie restriction prevents the early onset of T-cell senescence and thus helps ward off infectious diseases even at old age.