>  >, I would like
>>to know more about any work being done in investigations into causal
>>relationships and the biological mechanisms behind casein allergies and
>>intolerances.
>
A quick search thru an article database  on Casein + allergy revealed
the following latest journal articles:

Record 1 of 10 in Biological Abstracts 2001/07-2001/12

TI:  Elevated serum concentrations of beta-tryptase, but not
alpha-tryptase, in Sudden Infant Death Syndrome (SIDS). An
investigation of anaphylactic mechanisms.
AU:  Buckley-M-G; Variend-S; Walls-A-F {a}
SO:  Clinical-and-Experimental-Allergy. [print] November, 2001; 31
(11): 1696-1704.
PY:  2001
LA:  English
AB:  Background Sudden Infant Death Syndrome, (SIDS) or cot death,
remains the most common category of post-perinatal death in the UK.
By definition, the cause of death is unknown, but a long-standing
theory is that some of these deaths could be the result of
anaphylaxis. Objective To investigate the potential contribution of
anaphylactic mechanisms to deaths in infancy by determining relative
levels of alpha- and beta-tryptases and both total and
allergen-specific IgE in sera from groups of infants whose deaths
were attributed to SIDS or to other causes. Methods Serum samples
were collected at the time of post-mortem examination from infants
whose death was classed as SIDS (n = 40) and from a comparison group
in which cause of death had been established (n = 32). Serum tryptase
concentrations were measured with a radioimmunoassay with monoclonal
antibody G5 which detects primarily beta-tryptase or an ELISA with
antibody AA5 which has equal sensitivity for alpha- and
beta-tryptases. Levels of total IgE and IgE specific for casein,
beta-lactoglobulin, house dust mite and moulds were determined.
Results Analysis of the results of the two assays for tryptase
indicated that levels of the beta-like tryptase (the form secreted on
anaphylactic degranulation) were significantly higher in serum from
infants with SIDS compared with those whose death was explained.
There was no evidence for an increase in serum levels of
alpha-tryptase (the variant secreted constitutively from mast cells).
Total levels of serum IgE did not differ between the two groups and,
reflecting the low circulating IgE concentrations in infancy, an
elevation in IgE specific for the panel of allergens was not
detected. Conclusions In a proportion of SIDS victims there may be
increased serum levels of beta-like tryptase, a marker for
anaphylaxis. The failure to detect an increase in alpha-tryptase
would suggest that mast cell hyperplasia is not a feature of cot
death. The nature of the inciting agents remains unclear, but
anaphylaxis deserves serious consideration as a possible cause of
sudden death in infancy.
AN:  200100364059
UD:  20011206

Record 2 of 10 in Biological Abstracts 2001/07-2001/12

TI:  Identification of IgE and IgG binding epitopes on beta- and
kappa-casein in cow's milk allergic patients.
AU:  Chatchatee-P; Jarvinen-K-M; Bardina-L; Vila-L; Beyer-K; Sampson-H-A {a}
SO:  Clinical-and-Experimental-Allergy. [print] August, 2001; 31 (8):
1256-1262.
PY:  2001
LA:  English
AB:  Background: Cow's milk allergy (CMA) affects 2.5% of children
aged less than 2 years of age. Although beta- and kappa-casein are
considered among the major allergens responsible for CMA, no data are
available on their allergenic epitopes in humans. Objective: The aim
of the study was to identify IgE- and IgG-binding epitopes on beta-
and kappa-casein and to determine whether the pattern of epitope
recognition is associated with the natural history of CMA. Methods:
Overlapping decapeptides representing the entire length of beta- and
kappa-casein, respectively, were synthesized on a
cellulose-derivatized membrane. Sera from 15 milk-allergic children,
4-18 years of age, with high levels of specific IgE antibodies to
cow's milk were used to identify IgE- and IgG-binding epitopes. In
addition, IgE epitopes were screened with pooled or individual sera
from younger patients aged less than 3 years and who had low levels
of specific serum IgE, who are likely to outgrow CMA. Resu!
lt!
s: Six major and three minor IgE-binding epitopes, as well as eight
major and one minor IgG binding regions, were identified on
beta-casein. Eight major IgE-binding epitopes, as well as two major
and two minor IgG-binding epitopes, were detected on kappa-casein.
Three of the IgE binding regions on beta-casein and six on
kappa-casein were recognized by the majority of patients in the older
age group, but not by the younger patients. Conclusion: Information
regarding the immunodominant epitopes in beta- and kappa-casein may
be important for understanding the pathophysiology and natural
history of CMA. Differences in epitope recognition may be useful in
identifying children who will have persistent milk hypersensitivity.
AN:  200100283859
UD:  20010830