I’ve saved 229 papers from 2007 in my References database. Here are some of the ones I was especially struck by this year. This doesn’t necessarily mean “most significant”, or “most dramatic”, or anything other than “I thought they were cool”.
Twelve papers — one per month1 — in alphabetical order so I don’t have to decide between them:
1. Apetoh, L., Ghiringhelli, F., Tesniere, A., Obeid, M., Ortiz, C., Criollo, A. et al. (2007). Toll-like receptor 4-dependent contribution of the immune system to anticancer chemotherapy and radiotherapy. Nat Med, 13, 1050 – 1059.
Suggests that the real reason chemotherapy works is not that it kills the tumor cells, but rather that the tumor cells are rendered capable of priming the adaptive immune system; it’s the immune system that actually does the work of killing off the tumor. I talked about this paper here.
|“Crow 104” by Meggan Gould|
2. Brault, A. C., Huang, C. Y., Langevin, S. A., Kinney, R. M., Bowen, R. A., Ramey, W. N. et al. (2007). A single positively selected West Nile viral mutation confers increased virogenesis in American crows. Nat Genet, 39(9), 1162-1166.
An example of how a small change in a viral genome can make a huge change in its pathogenesis — this West Nile virus mutant is more lethal to crows. Read this one in conjunction with LaDeau, S. L., Kilpatrick, A. M., & Marra, P. P. (2007). West Nile virus emergence and large-scale declines of North American bird populations. Nature, 447(7145), 710-713. I talked about West Nile Virus here, though not so much about these papers.
3. Flutter, B., Fu, H. M., Wedderburn, L., & Gao, B. (2007). An extra molecule in addition to human tapasin is required for surface expression of Î²2m linked HLA-B4402 on murine cell. Mol Immunol, 44(14), 3528-3536.
Evidence that there is still at least one unidentified molecule that’s important for antigen presentation. Mainly interesting to me because it reflects my own paper from 2005 that shows the same thing. The description of this phenotype isn’t identical to my mutant cell line, but I suspect it’s the same molecule.
4. Garrison, K. E., Jones, R. B., Meiklejohn, D. A., Anwar, N., Ndhlovu, L. C., Chapman, J. M. et al. (2007). T Cell Responses to Human Endogenous Retroviruses in HIV-1 Infection. PLoS Pathog, 3(11), e165.
Endogenous retroviruses, the withered corpses of ancient retroviruses that litter our genome, are partially reanimated by HIV infection. The newly-expressed HERV proteins are recognized by T cells, potentially offering a non-mutating target that might enable T cells to recognize HIV-infected cells.
|Blood vessels in a colorectal cancer|
5. Koebel, C. M., Vermi, W., Swann, J. B., Zerafa, N., Rodig, S. J., Old, L. J. et al. (2007). Adaptive immunity maintains occult cancer in an equilibrium state. Nature, 450(7171), 903-907.
Cancers arise from normal cells through a multi-step process; immune system evasion is one critical step in this process. It’s been proposed that nascent cancers may spend years in an undetectable state, suppressed by the immune system. Here is more or less direct evidence for this equilibrium state. I talked about this paper here and here .
6. Kotturi, M. F., Peters, B., Buendia-Laysa, F. J., Sidney, J., Oseroff, C., Botten, J. et al. (2007). The CD8+ T-cell response to lymphocytic choriomeningitis virus involves the L antigen: uncovering new tricks for an old virus. J Virol, 81(10), 4928-4940.
Mainly a technological advance in T cell epitope identification, but a dramatic example of how much there is to learn even in this very well-studied virus system. Also offers a really dramatic example of immunodominance. I talked about it here, among other places.
7. Munks, M. W., Pinto, A. K., Doom, C. M., & Hill, A. B. (2007). Viral interference with antigen presentation does not alter acute or chronic CD8 T cell immunodominance in murine cytomegalovirus infection. J Immunol, 178(11), 7235-7241.
Viruses have long been known to block the class I major histocompatibility complex antigen presentation pathway, and the presumption has been that this allows the virus to avade detection and destruction by cytotoxic T cells. But this has mainly been a presumption because the work is mainly in cultured cells, rather than in real animals. Here Ann Hill’s group continues their work looking at immune evasion molecules in authentic infections — and show that they have amazingly little impact on the infection or the immune response. I talked about it here.
8. Siddle, H. V., Kreiss, A., Eldridge, M. D., Noonan, E., Clarke, C. J., Pyecroft, S. et al. (2007). Transmission of a fatal clonal tumor by biting occurs due to depleted MHC diversity in a threatened carnivorous marsupial. Proc Natl Acad Sci U S A, 104(41), 16221-16226.
Tasmanian Devils are being killed by an infectious tumor, which apparently can spread because Devils are not very diverse at their major histocompatibility complex region — the region that usually serves to prevent graft “takes”, which is essentially what this tumor is doing. I discussed this paper here, along with the even more interesting canine transmissible venereal tumor.
9. Stemberger, C., Huster, K., M., Koffler, M., Anderl, F., Schiemann, M., Wagner, H. et al. (2007). A Single Naive CD8+ T Cell Precursor Can Develop into Diverse Effector and Memory Subsets. Immunity, 27(6), 985-997.
How many T cells are there that recognize a particular antigen, and how much expansion do they undergo to form the immune response we all know and love? I talked about a previous paper that counted T cells — here is evidence that a single cell can form multiple branches of an immune response.
|Electron tomogram of HSV2|
10. Verjans, G. M., Hintzen, R. Q., van Dun, J. M., Poot, A., Milikan, J. C., Laman, J. D. et al. (2007). Selective retention of herpes simplex virus-specific T cells in latently infected human trigeminal ganglia. Proc Natl Acad Sci U S A, 104(9), 3496-3501.
Herpes simplex virus has traditionally been believed to enter a latent state in human trigenimal ganglia during which no viral proteins are produced. This paper is one of a series that shows that the immune system recognizes neurons latently infected with HSV, which strongly suggests that there is some very low-level protein expression, offering a mechanism by which the virus can interact with the world outside its neuron. I talked about it here.
11. Wearsch, P. A. & Cresswell, P. (2007). Selective loading of high-affinity peptides onto major histocompatibility complex class I molecules by the tapasin-ERp57 heterodimer. Nat Immunol, 8(8), 873-881.
After years of trying, here at last is efficient in vitro MHC class I peptide loading. I talked about it here.
12. Zhang, S.-Y., Jouanguy, E., Ugolini, S., Smahi, A., Elain, G., Romero, P. et al. (2007). TLR3 Deficiency in Patients with Herpes Simplex Encephalitis. Science, 317(5844), 1522-1527.
Herpes simplex encephalitis is a rare, but devastating, complication of herpes simplex infection. Here Zhang et al show that a defect in TLR3 — not generally associated with HSV — is associated with this disease. I talked about the paper here.