Appendix is not even redundant, let alone not vestigial?
|December 3, 2015||Posted by News under Intelligent Design, News, vestigial organs|
So says some new research. First, remember “vestigial organs”?
Being teens, we never considered the implications of the fact that the proposition is never supposed to work the other way. That is, now that almost all such organs have been found to be functional (so far), the no-design PR lobby just moved to other claims. For example, junk DNA!
Immune cells make appendix ‘silent hero’ of digestive health
“Popular belief tells us the appendix is a liability,” she said. “Its removal is one of the most common surgical procedures in Australia, with more than 70,000 operations each year. However, we may wish to rethink whether the appendix is so irrelevant for our health.
Note: Decades ago, appendicitis was often not diagnosed until removal was the only life-saving option.
“We’ve found that ILCs [innate lymphoid cells] may help the appendix to potentially reseed ‘good’ bacteria within the microbiome — or community of bacteria — in the body. A balanced microbiome is essential for recovery from bacterial threats to gut health, such as food poisoning.”
“We found ILCs are part of a multi-layered protective armoury of immune cells that exist in healthy individuals. So even when one layer is depleted, the body has ‘back ups’ that can fight the infection.
“Redundant”: A frequent feature of living systems, as well as human artifacts. If one level fails, another kicks in. Sometimes marketed to the public as evidence against design.
Note: Here is some post-vestigial organ spin from one of Darwin’s folk.
See also: “Vestigial” whale, dolphin hip bones actually needed for, um, reproduction
Is vestigial organ a term that should be retired?
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Here’s the abstract:
Intestinal T cells and group 3 innate lymphoid cells (ILC3 cells) control the composition of the microbiota and gut immune responses. Within the gut, ILC3 subsets coexist that either express or lack the natural cytoxicity receptor (NCR) NKp46. We identified here the transcriptional signature associated with the transcription factor T-bet–dependent differentiation of NCR- ILC3 cells into NCR+ ILC3 cells. Contrary to the prevailing view, we found by conditional deletion of the key ILC3 genes Stat3, Il22, Tbx21 and Mcl1 that NCR+ ILC3 cells were redundant for the control of mouse colonic infection with Citrobacter rodentium in the presence of T cells. However, NCR+ ILC3 cells were essential for cecal homeostasis. Our data show that interplay between intestinal ILC3 cells and adaptive lymphocytes results in robust complementary failsafe mechanisms that ensure gut homeostasis. (paywall) – Lucille C Rankin, Mathilde J H Girard-Madoux, Cyril Seillet, Lisa A Mielke, Yann Kerdiles, Aurore Fenis, Elisabeth Wieduwild, Tracy Putoczki, Stanislas Mondot, Olivier Lantz, Dieter Demon, Anthony T Papenfuss, Gordon K Smyth, Mohamed Lamkanfi, Sebastian Carotta, Jean-Christophe Renauld, Wei Shi, Sabrina Carpentier, Tim Soos, Christopher Arendt, Sophie Ugolini, Nicholas D Huntington, Gabrielle T Belz, Eric Vivier. Complementarity and redundancy of IL-22-producing innate lymphoid cells. Nature Immunology, 2015; DOI: 10.1038/ni.3332
This vid begins by stating in no uncertain terms that we learned in school that the appendix was useless: