NEWS & VIEWS RESEARCH
good reason for not trusting quantum devices:
they are extremely fragile, complex and dif-
ficult to control. Can we leash the ‘quantum
tiger’? Can we test whether complex quantum
systems behave as they should, while trusting
only our good old classical devices? Reichardt
and colleagues prove that, miraculously, the
answer is yes.
The authors’ starting point is the CHSH
game3, in which two non-communicating
parties play against a referee (see Fig. 2 of the
paper1). Classical players can win only 75% of
the time, but if they share a special quantum
state known as the Einstein–Podolsky–Rosen
(EPR) quantum state their probability of win-
ning becomes 85%. This result is a manifesta-
tion of what Einstein called “spooky action at
a distance”, also known as quantum entangle-
ment. It provides a way of testing whether a
non-communicating two-party system is in
a quantum-mechanical state: play the CHSH
game repeatedly, each time with the same ini-
tial state, and see whether the players win more
than 75% of the games.
Now, let’s reverse this logic. It turns out
that if the players win 85% of the games, then
their initial shared state must have been the
EPR state. The main technical contribution
of Reichardt et al. is a robust, multi-game
version of this claim: if the two players play
many CHSH games in sequence, starting with
a shared multi-particle initial state, and win
close to the optimal 85% of the games, then the
entire initial state of the two players must be
close to a collection of many independent EPR
states. This implies much more than verifying
the ‘quantumness’ of a system — it certifies
a particular state of a large entangled quan-
tum system, and it does so simply by posing
a sequence of classical ‘questions and answers’
to the system being tested (Fig. 1).
Certifying entanglement of many-particle
quantum systems has an important implication
for high-security cryptography. Quantum-key
distribution (QKD)7, the pinnacle of quantum
cryptography, is a protocol that, remarkably,
allows two parties to communicate secretly
even if the entire world is trying to eavesdrop.
However, realizations of this protocol are not
automatically secure because of imperfections
in the devices. For example, the first QKD appa-
ratus8 emitted sounds that revealed information
about the secrets being communicated, render-
ing it secure only against deaf eavesdroppers.
Implementations of QKD have repeatedly been
found to be insecure and to require corrections
because of such issues. In 1998, Mayers and Yao
envisioned9 using entanglement certification
to achieve ‘device-independent’ QKD, which
is secure even if the quantum devices that are
used by the two parties to communicate were
manufactured by the eavesdropper herself.
After 15 years of important but partial progress
by other researchers, Reichardt and colleagues
have finally made the missing theoretical leap
towards this goal: they describe a QKD protocol
Output 0 1
Input 0 1
Figure 1 | Classical interaction with a quantum
system.  Reichardt et al.1 model an arbitrarily
complex quantum system as a ‘black box’
with simple classical inputs and outputs. An
experimentalist can probe the system only by
pushing button 0 or button 1, and the system
outputs only two possible answers, 0 or 1,
corresponding to the left or right light flashing.
and prove that it is secure even when the devices
have been maliciously designed.
But there is more to it. The authors’ proto-
col can be extended to certify the correct time-
evolution of entanglement into quantum states
that are considerably more complex than a
collection of independent EPR states. In other
words, their extended protocol certifies that a
general quantum computation was performed
as claimed. How can a classical experimentalist
verify that such quantum states are generated
even though they are much too complex for
him or her to write down? This task has previ-
ously been achieved10 using a ‘slightly quan-
tum-mechanical’ test. Reichardt et al. cleverly
AU TO I M M U N I T Y
Rubbing salt in
the wound
The ability of sodium chloride to induce enzymatic activity that leads to the
generation of pathogenic TH17 immune cells implicates salt as a possible factor
that might exacerbate autoimmune disease. See Letters p.513 & p.518
JOHN J. O’SHEA & RUSSELL G. JONES
T
he role of the immune system is to pro-
tect our bodies from viral, bacterial,
fungal and parasitic infections. But,
sophisticated as this system is, it can go awry.
One consequence is autoimmunity, a diverse
collection of disorders in which the immune
system turns against the host. Genetics and
gender undoubtedly play key parts in the
2 5 A P R I L 2 0 1 3 | VO L 4 9 6 | NAT U R E | 4 3 7
© 2013 Macmillan Publishers Limited. All rights reserved
provide a completely classical test, using an
approach similar to that of a policewoman
interrogating two thieves about a crime she
knows nothing about; she looks for incon-
sistencies in their answers, preventing them
from coordinating. The only assumptions in
the authors’ work are that the quantum com-
puter being tested can be divided into two
non-interacting parts, and that the tester can
communicate privately with each part.
Reichardt and colleagues’ protocols are yet
to be made practical, that is, fault tolerant and
more efficient. However, they provide a proof
of principle that hands-off testing of the inner
workings of arbitrarily complex quantum
systems is possible. Implementing these pro-
tocols will allow new and considerably more
stringent tests of quantum-information-pro-
cessing devices than previously performed. ■
Dorit Aharonov is in the School of Computer
Science & Engineering, The Hebrew University
of Jerusalem, 91904 Jerusalem, Israel.
e-mail: doria@cs.huji.ac.il
1. Reichardt, B. W., Unger, F. & Vazirani, U. Nature
496, 456–460 (2013).
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3. Clauser, J. F., Horne, M. A., Shimony, A. & Holt, R.
Phys. Rev. Lett. 23, 880–884 (1969).
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455304 (2012).
6. Aharonov, D. & Vazirani, U. in Computability: Turing,
Godel, Church, and Beyond (eds Copeland, B. J.,
Posy, C. J. & Shagrir, O.) (MIT press, in the press).
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Comp. Sci., Beijing, 453–469 (Tsinghua Univ. Press,
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susceptibility to autoimmune diseases, but
environmental factors are also important. In
this issue, Kleinewietfeld et al.1 (page 518)
and Wu et al.2 (page 513) provide provocative
data implicating a novel component in this
mix: salt*.
The stories focus on a crucial orchestra-
tor of immune responses — the CD4+, or
*This article and the papers under discussion1,2 were
published online on 6 March 2013.
 RESEARCH NEWS & VIEWS
a b IL-23
IL-23R
↑ TH17 cells
High-salt
↑ EAE onset Other
diet
↑ EAE severity cytokines NaCl
PI3K
Akt PDK1 p38
Normal ↓ TH17 cells mTOR
diet SGK1 NFAT5
↓ EAE severity
T-cell SGK1–/– ↓ O2 HIF-α
RORγT IL-23R
Nutrients Glycolysis
IL-17A IL-17F
High-salt Protection
diet from EAE
T-cell SGK1–/– Pathogenic
TH17 phenotype
Figure 1 | SGK1 and the differentiation of TH17 cells.  a, Kleinewietfeld et al.1 and Wu et al.2 provide
evidence that a high-salt diet can enhance the differentiation of a class of immune cell called TH17 cells,
and exacerbate disease in a mouse model of multiple sclerosis called experimental autoimmune
encephalitis (EAE). They also show that mice whose T cells lack the enzyme SGK1 (T-cell SGK −/−) display
reduced disease severity and are protected from NaCl-exacerbated EAE. b, The authors demonstrate that
extracellular NaCl concentration and signalling through the IL-23 receptor both influence the activity
of SGK1 to drive expression of pathogenic TH17-cell characteristics, which include the production
of the cytokines IL-17A and IL-17F and enhanced expression of the IL-23 receptor (IL-23R) and the
transcription factor RORγT (encoded by Rorc). However, this finding must be considered in the context
of other environmental factors, such as oxygen and nutrient provision. These influence signalling
pathways and glycolytic metabolism in ways that regulate not only TH17-cell differentiation, but also that
of other classes of T cell.
‘helper’, T cells. These cells regulate immune This makes sense, because p38 is an evolu-
responses through their ability to differenti- tionarily conserved kinase that is activated by
ate into distinct classes of cell according to the changes in cellular osmolarity, and NFAT5 and
nature of the offending pathogen. In the past SGK1 are both substrates of p38.
decade, increasing attention has focused on a The authors also find that SGK1 is
subset of CD4+ T cells, commonly known as expressed in TH17 cells and is induced by
T helper 17 (TH17) cells3–6, which secrete mol- NaCl, and show that mice lacking this kinase
ecules belonging to the IL-17 group of cell- in their T cells have impaired expression of
signalling compounds called cytokines. Cells IL-17-family cytokines and of a receptor for
that produce IL-17 are prominent in the gut, another cytokine molecule, IL-23. When they
where they influence its barrier function and tested these knockout mice in the EAE model,
help to protect against extracellular pathogens they found that the lack of SGK1 also leads
and fungi. However, these helpers can also be to reduced neuropathology. SGK1 has been
traitors — TH17 cells are important drivers of implicated in inflammatory pathways before: it
autoimmune disease, and have inflammatory is known to inactivate the transcription factor
properties. Foxo1. Accordingly, Foxo1-deficient T cells
The present studies tell their stories in have higher levels of IL-17 and IL-23-receptor
different ways, but both show that an ele- expression.
vated sodium chloride (NaCl) concentration In considering these studies, it is appropriate
(40–80 millimolar) in an otherwise isotonic to re-emphasize that IL-17 and TH17 cells are
culture medium promotes the differentiation not always the villains; they also protect us from
of CD4+ T cells into TH17 cells in vitro. Perhaps a universe of true villains. In the same vein, it
the most provocative experiments relate to an should also be pointed out that not all TH17
in vivo correlate of this finding. The authors cells are alike: although some IL-17-producing
demonstrate that a high-salt diet accelerates T cells mediate immune pathology, others do
neuropathology in experimental autoimmune not. IL-23 is a key cytokine in generating patho-
encephalomyelitis (EAE), a mouse model of the genic TH17 cells7, and the authors of both papers
autoimmune disease multiple sclerosis. They note that NaCl and SGK1 seem to contribute to
used inhibitors, interfering RNA molecules the generation of TH17 cells that have patho-
and knockout mice to test the role of cellular genic potential. However, many cells other
signalling pathways in these processes, and link than CD4+ T cells, including innate immune
the regulation of NaCl and TH17 differentiation cells and γ/δ T cells, also produce IL-17 and
with the transcription factor NFAT5 and the related cytokines8. Although a high-salt diet
protein-kinase enzymes p38 and SGK1 (Fig. 1). may indeed worsen autoimmune disease,
4 3 8 | NAT U R E | VO L 4 9 6 | 2 5 A P R I L 2 0 1 3
© 2013 Macmillan Publishers Limited. All rights reserved
the data provided do not establish exactly
which cells NaCl works on to achieve this.
An additional point is that autoimmune
diseases are heterogeneous, and the benefit
achieved by blocking IL-17 is variable. Inhib-
iting IL-17 is useful in treating psoriasis, but
less so in inflammatory bowel disease; the jury
is still out on whether targeting IL-17 will be
of help in treating multiple sclerosis. It is also
worth noting that the studies by Kleinewietfeld
et al.1 and Wu et al.2 show that NaCl exacer-
bates an artificially created disease; there are
no data indicating that dietary salt promotes
or worsens spontaneous disease.
The complex interaction of the factors that
regulate helper-T-cell differentiation must also
be taken into account when considering these
results (Fig. 1). SGK1 is a member of the AGC
family of protein kinases, and is homologous
to the enzyme Akt9. Akt has well-documented
effects on cell survival, metabolism and helper-
T-cell differentiation. Moreover, Akt and SGK1
share upstream activators, including the
enzymes PI3K and PDK1, and downstream
substrates. Key molecules, such as mTor and
Foxo1, are also influenced by diverse factors
and have complex effects on T-cell function10.
Furthermore, helper T cells are influenced
by nutrient availability and by the oxygen-
sensitive transcription factor HIF-1α, which
suggests a close link between metabolism and
differentiation. Similarly, p38 is also a rec-
ognized regulator of helper T cells11. This is
pertinent to the present studies, because the
authors’ results suggest that the functions of
SGK1 and NaCl are not entirely congruent:
SGK1 positively regulates IL-17, but negatively
regulates the genes Ifng, Tbx21 Il4, Il13, Gata3,
Il2 and Il9, whereas NaCl positively regulates
IL-17, Ifng, Tbx21, Il2 and Il9.
Thus, dietary salt is just one of many fac-
tors that influence helper T cells; cytokines,
the microbiota, diet, metabolism and other
diverse environmental factors are all impor-
tant too10,12,13. The bottom line is that these
kinases and transcription factors represent
key nodes for many receptors and signalling
pathways that integrate a vast array of stimuli.
So, although these are exciting and provoca-
tive data, it is clearly premature — as also
pointed out by both sets of authors — to state
that dietary salt influences autoimmune dis-
ease in humans and that this is mediated by
T-cell-induced production of IL-17. However,
the work should spur investigation of tangible
links between diet and autoimmune disease
in people. In doing so, it will be essential to
conduct formal, controlled clinical trials.
Fortunately, the risks of limiting dietary salt
intake are not great, so it is likely that several
such trials will be starting soon. ■
John J. O’Shea is in the Intramural Research
Program, National Institute of Arthritis and
Musculoskeletal and Skin Diseases, Bethesda,
Maryland 20892-1616, USA.

Russell G. Jones is at the Rosalind and
Morris Goodman Cancer Research Centre,
Department of Physiology, McGill University,
Montreal, Quebec H3G 1Y6, Canada.
e-mails: osheaj@arb.niams.nih.gov;
russell.jones@mcgill.ca
1. Kleinewietfeld, M. et al. Nature 496, 518–522 (2013).
2. Wu, C. et al. Nature 496, 513–517 (2013).
3. Weaver, C. T., Hatton, R. D., Mangan, P. R. &
Harrington, L. E. Annu. Rev. Immunol. 25, 821–852
(2007).
4. Stockinger, B., Veldhoen, M. & Martin, B. Semin.
Immunol. 19, 353–361 (2007).
5. Kolls, J. K. & Linden, A. Immunity 21, 467–476 (2004).
PART ICLE PHYSICS
Minimalism triumphant
The discovery of a particle that looked like the Higgs boson marked a milestone for
physics. Results reported since then are strikingly consistent with expectations for
the Higgs particle of the minimal standard model of particle physics.
FRANK WILCZEK
S
ince the announcement last July that a
new kind of particle had been discovered
at the Large Hadron Collider (LHC) at
CERN, Europe’s particle-physics laboratory
near Geneva in Switzerland, a much fuller
portrait of that particle has emerged. The two
main experimental collaborations, ATLAS
and CMS, reported a host of measurements
in papers and presentations at last month’s
Moriond conference in La Thuile, Italy1,2. So
far, all results remain consistent with the inter-
pretation that the new particle is the Higgs
boson anticipated in the minimal implementa-
tion of electroweak symmetry breaking in the
standard model of particle physics.
The Higgs particle is a rare and fleeting
physical phenomenon. Even at the LHC,
the particle is produced in less than one-bil-
lionth of the proton–proton collisions, and
it is highly unstable — its lifetime is inferred
to be about 10−22 seconds. To appreciate the
significance of the Higgs particle, it is neces-
sary to put it in its proper context — the Higgs
mechanism.
A central assumption of the standard model,
inferred from many experiments, is that the
basic forces of nature — the strong, weak and
electromagnetic forces, as well as gravity —
are mediated by quantum fields of spin 1 or
(for gravity) spin 2. It is challenging to accom-
modate that assumption theoretically, in
consistent equations. Naive attempts founder
because they predict the existence of violent
(quantum) fluctuations in the fields at short
distances, which lead to a plague of math-
ematical infinities in calculations of physical
quantities. These difficulties can be avoided
only in theories in which the fields have
NEWS & VIEWS RESEARCH
6. Miossec, P. & Kolls, J. K. Nature Rev. Drug Discov. 11,
763–776 (2012).
7. Cua, D. J. et al. Nature 421, 744–748 (2003).
8. Sutton, C. E., Mielke, L. A. & Mills, K. H. G. Eur. J.
Immunol. 42, 2221–2231 (2012).
9. Bruhn, M. A., Pearson, R. B., Hannan, R. D. &
Sheppard, K. E. Growth Factors 28, 394–408
(2010).
50 Years Ago
10. Honda, K. & Littman, D. R. Annu. Rev. Immunol. 30,
759–795 (2012).
11. Dong, C., Davis, R. J. & Flavell, R. A. Annu. Rev.
Immunol. 20, 55–72 (2002).
12. Wang, R. & Green, D. R. Nature Immunol. 13,
907–915 (2012).
‘Internal circulations within
13. Stockinger, B., Hirota, K., Duarte, J. & Veldhoen, M. liquid drops’ — It has long
Semin. Immunol. 23, 99–105 (2011). been recognized that under
certain conditions some sort of
axisymmetric flow is induced within
liquid drops as they pass through
a viscous medium … Although an
internal circulation theory has been
very attractive in considerations of
meteorological phenomena, there
appears to be little experimental
evidence to substantiate such a
theory … In this communication we
discuss a technique which affords
velocity measurements and at the
same time outlines the vortical
enormous symmetry, called gauge symmetry. core … The streamlines within the
Gauge symmetry, however, seems to require drop are recorded photographically
that the most basic manifestations of the gauge by means of dye trails. The figure
fields, the minimal concentrations of energy indicates
or quanta of the fields, are particles with zero the
mass. That property holds true in many cases: streak-
the photons of electromagnetism, the colour lines due
gluons of the strong interaction and the gravi- to the
ton of gravity do seem to have zero mass. But motion
W and Z bosons, the quanta of the fields that within
are responsible for the weak interaction, have water
substantial masses. drops
The Higgs mechanism provides a way out moving through mineral oil … We
of this difficulty. The key observation is that have obtained a great deal of velocity
gauge symmetry requires the W and Z bosons data with this method.
to have zero mass only in empty space. Mater­ From Nature 27 April 1963
ial can slow them down, screen their influence
and make them behave as if they have non-zero
mass. If an appropriate mater­ial fills all space
uniformly and stably, the W and Z bosons will
never escape its influence — and they will
100 Years Ago
always be observed to have non-zero mass. The The twinkling of stars may be
hypothesis that such a material does, in fact, imitated in the dark-room. If a
fill space is the essence of the Higgs mecha- small light be looked at in a dark-
nism. But does this material exist? And, if so, room, as, for instance, that coming
what is it made out of? through the smallest diaphragm of
The triumph of the standard-model my colour perception lantern, …
account of weak interactions, which relies care being taken not to move the
on the Higgs mechanism, has long provided eye, the light will appear to twinkle
overwhelming, if circumstantial, evidence like a star. It will be noticed that
that the mater­ial exists. In recent months, we pale bluish-violet circles start at the
have learned what it is made out of. Among periphery of the field of vision, and,
all the logical possibilities for the new mater­ gradually contracting, reach the
ial, the simplest and most economical pro- centre. On reaching the centre the
posal defines the ‘minimal standard model’. light brightens. If the circles stop
In this model, the cosmic material is made the light disappears. The colour of
from just one ingredient. The terminology in the circle is the same for white light
this subject is both confused and in flux, but or any colour.
here the term Higgs particle is used to refer From Nature 24 April 1913
to the unique particle that is introduced to
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© 2013 Macmillan Publishers Limited. All rights reserved