B cell immunology — ZBTB38 transcription factor

A 25-minute acid treatment (pH 5.7) would turn mouse blood cells into pluripotent stem cells, as Obokata et al. (2014) reported.

Acid-treated spleen cells from newborn Oct4-GFP mice did not express the stem cell marker Oct4-GFP after 3 to 6 days, and qPCR found no rise in Oct4, Sox2 or Nanog. Lung fibroblasts gave the same result.

Why it matched: similar wording · failed the same way: Held in the model species, not beyond it

Intranodal injections of tumour-antigen-loaded autologous CD1c+ and plasmacytoid dendritic cells after surgery would lengthen recurrence-free survival in resected stage IIIB/C melanoma.

In the randomised MIND-DC trial (148 patients, 99 nDC vs 49 placebo), 2-year recurrence-free survival was 36.8% with nDCs versus 46.9% with placebo (p = 0.31); median RFS 12.7 vs 19.9 months (HR 1.25), and overall survival did not differ.

Why it matched: mechanism: Adaptive immunity & tolerance · failed the same way: Held in the model species, not beyond it

Immunising mice with CCR6 peptides or CCR6-expressing cells would produce monoclonal antibodies that block the receptor from binding its ligand CCL20.

Peptide immunisation produced no antibodies that recognised the native receptor. Cell immunisation produced CCR6-specific antibodies, but none blocked CCL20 binding.

Why it matched: similar wording · failed the same way: Held in the model species, not beyond it

Low-dose IL2 raises regulatory T cells, which reverse protein loss in the urine in animal models of nephrotic syndrome, so it would lower protein loss in children whose nephrotic syndrome resists all other drugs.

In 5 boys given six monthly cycles, IL2 raised regulatory T cells in some, but protein in the urine and kidney function did not change at any point. One child had an asthma attack after the first dose.

Why it matched: mechanism: Adaptive immunity & tolerance · failed the same way: Held in the model species, not beyond it

A mouse model of breast cancer driven by polyoma middle T antigen would reproduce the systemic changes in monocytes seen in human breast cancer, making it a usable model for studying them.

Tumour-bearing mice did show more monocytes in bone marrow, blood and spleen, from faster proliferation, and transcriptional changes in classical monocytes led by down-regulated type I interferon signalling and antigen presentation. But these transcriptome changes did not match those found in patients with breast cancer.

Why it matched: mechanism: Gene expression & RNA · failed the same way: Held in the model species, not beyond it